Cerebral infarction and thrombotic meningoencephalitis in a calf due to candidiasis / Infarto cerebral e meningoencefalite trombótica em um bezerro devido a candidíase

We described a case of cerebral infarction and thrombotic meningoencephalitis due to candidiasis in a seven-month-old calf. The death occurred three days after the onset of apathy, fever, and the head's lateral deviation to the left. Macroscopic changes in the brain consisted of asymmetry of telencephalic hemispheres; the right hemisphere was enlarged, causing cerebellar herniation. A focally extensive red area was observed on the surface of the right occipital lobe. At cross-sections of the fixed brain, the lesions revealed to be extensive, red-brown, soft or cavitated areas affecting the white and grey matter from the level of the thalamus to the cerebellum and compressing subjacent structures. Histologically, there was acute, coalescent, multifocal necrosupurative meningoencephalitis, associated with vasculitis, congestion, thrombosis, edema, infarction, and intralesional fungal hyphae. The diagnosis of cerebral infarction and thrombotic meningoencephalitis due to candidiasis was made by the pathological changes, the staining and morphological characteristics of the agent, and immunohistochemistry. The cerebral infarction and thrombotic meningoencephalitis in cattle can result from vascular lesions due to infection by Candida sp.; although uncommon, this case demonstrated that candidiasis should be part of a list of differential diagnoses of severe brain injuries in cattle.

Descreve-se um caso de infarto cerebral e meningoencefalite trombótica devido a candidíase em um bezerro de sete meses de idade. A morte ocorreu três dias após o início de apatia, febre e desvio lateral da cabeça para a esquerda. As alterações macroscópicas no cérebro consistiam em assimetria dos hemisférios telencefálicos; o hemisfério direito estava aumentado, causando herniação cerebelar. Uma extensa área vermelha focal foi observada na superfície do lobo occipital direito. Nos cortes transversais do encéfalo fixado, as lesões revelaram áreas extensas, marrom-avermelhadas, moles ou cavitadas, afetando a substância branca e cinzenta desde o nível do tálamo até o cerebelo e comprimindo as estruturas subjacentes. Histologicamente, havia meningoencefalite necrossupurativa multifocal aguda, coalescente, associada a vasculite, congestão, trombose, edema, infarto e hifas fúngicas intralesionais. O diagnóstico de infarto cerebral e meningoencefalite trombótica devido a candidíase foi feito pelas alterações patológicas, coloração e características morfológicas do agente e imuno-histoquímica. O infarto cerebral e meningoencefalite trombótica em bovinos pode resultar de lesões vasculares devido à infecção por Candida sp.; embora incomum, este caso demonstra que a candidíase deve fazer parte de uma lista de diagnósticos diferenciais de lesões cerebrais graves em bovinos.

Astragaloside IV alleviates stroke-triggered early brain injury by modulating neuroinflammation and ferroptosis via the Nrf2/HO-1 signaling pathway

Purpose: Stroke is an acute cerebrovascular disease. Astragaloside IV (AS-IV) is an active ingredient extracted from Astragalus membranaceus with an established therapeutic effect on central nervous system diseases. This study examined the neuroprotective properties and possible mechanisms of AS-IV in stroke-triggered early brain injury (EBI) in a rat transient middle cerebral artery occlusion (MCAO) model. Methods: The neurological scores and brain water content were analyzed. 2,3,5-triphenyl tetrazolium chloride (TTC) staining was utilized to determine the infarct volume, neuroinflammatory cytokine levels, and ferroptosis-related genes and proteins, and neuronal damage and molecular mechanisms were evaluated by terminal deoxynucleotidyl transferase dutp nickend labeling (TUNEL) staining, western blotting, and real-time polymerase chain reaction. Results: AS-IV administration decreased the infarct volume, brain edema, neurological deficits, and inflammatory cytokines TNF-α, interleukin-1ß (IL-1ß), IL-6, and NF-κB, increased the levels of SLC7A11 and glutathione peroxidase 4 (GPX4), decreased lipid reactive oxygen species (ROS) levels, and prevented neuronal ferroptosis. Meanwhile, AS-IV triggered the Nrf2/HO-1 signaling pathway and alleviated ferroptosis due to the induction of stroke. Conclusion: Hence, the findings of this research illustrate that AS-IV administration can improve delayed ischemic neurological deficits and decrease neuronal death by modulating nuroinflammation and ferroptosis via the Nrf2/HO-1 signaling pathway.

Effects of local and remote ischemic postconditioning methods on ischemiareperfusion injury in a young animal model of acute mesenteric ischemia

Purpose: Acute mesenteric ischemia (AMI) is a condition in pediatric surgery that ranges from intestine necrosis to death. Ischemic postconditioning (IPoC) methods were developed to reduce the damage caused by revascularization. This study aimed to evaluate the efficacy of these methods in an experimental weaning rat model. Methods: Thirty-two 21-day-old Wistar rats were allocated into four groups according to the surgical procedure performed: control, ischemia-reperfusion injury (IRI), local (LIPoC) and remote IPoC (RIPoC). At euthanasia, fragments of the intestine, liver, lungs, and kidneys were submitted to histological, histomorphometric, and molecular analyses. Results: In the duodenum, intestines, and kidneys histological alterations promoted by IRI were reversed by remote postconditioning method. In the distal ileum, the histomorphometric alterations could be reversed by the postconditioning methods with more evident effects promoted by the remote method. The molecular analysis found that the levels of expression of Bax (proapoptotic) and Bcl-XL (antiapoptotic) genes in the intestine were increased by IRI. These alterations were equally reversed by the postconditioning methods, with more evident effects of the remote method. Conclusions: IPoC methods positively reduced the damage caused by IRI in weaning rats.

Impact of high-fat diet consumption during prolonged period of pregnancy on placenta structures and umbilical vascular growth in goats

This study aimed to verify the impact of high-fat diet consumption for a prolonged period on oxidative stress, fetal growth, umbilical vascular system, and placental structures in pregnant goats. Twenty-two pregnant goats were grouped into the control diet (n= 11) and fat diet (n = 11). Flaxseed meal was added to the fat diet, replacing the corn grain of concentrate, from gestational day 100 to delivery date. Diets were isonitrogenous and isoenergetic, differing in fat content (2.8% vs. 6.3% dry matter). The fat group showed higher feed intake and total plasma lipid levels than the control group (P < 0.001). No difference was found in placentome, and umbilical vascular development. Fat diet-fed goats exhibited a lower systolic peak in the umbilical artery. At delivery, placental traits were similar with the exception of the cotyledon width (P = 0.0075), which was smaller in the fat group and cotyledon surface (P = 0.0047) for multiple pregnancy of fat diet. Cotyledonary epithelium showed more intense staining of lipid droplets and a greater area for lipofuscin staining in the fat group compared to control group (P < 0.001). The mean live weight of the kids was lower in the fat group in the first week after delivery than in control group. Thus, in goats, the continuous administration of a high-fat diet during pregnancy does not appear to modify the fetal-maternal vascular structures but has an impact on a part of the placental structure; therefore, its use must be carefully evaluated.(AU)

B-mode and Doppler ultrasound of bitches' kidneys with mammary neoplasia submitted to adjuvant chemotherapy / Ultrassonografia modo-B e Doppler dos rins de cadelas com neoplasias mamárias submetidas à quimioterapia adjuvante

Mammary neoplasia represents the most frequently diagnosed type of neoplasia in bitches. Although surgical removal is the procedure of choice for therapeutic management, chemotherapy protocols appear as important allies and adjuvants. Despite the great advances that have occurred in the field of cancer therapy, the systemic repercussions of these drugs still impose important limitations on their use. In this sense, the development of increasingly targeted therapeutic protocols and preventive monitoring of patients represent important strategies to avoid possible complications - among them, Acute Kidney Injury (AKI). Routinely, ultrasound evaluation is used to identify morphological or metastatic variations in abdominal cavity organs. Acting complementary to the B-mode evaluation, Doppler mapping proves to be efficient in recognizing alterations in vascular hemodynamics. Therefore, the objective of the present study was to evaluate the use of B-mode and Doppler ultrasound to identify renal morphological and hemodynamic alterations in bitches with mammary neoplasia submitted to adjuvant chemotherapy protocols that associate gemcitabine with carboplatin. Thirteen bitches were included, without distinction of breed and between seven and 13 years of age. The animals were evaluated ultrasonographically at two different times during three consecutive chemotherapy cycles: before (T0) and one and a half hours after each cycle (T1), for 42 days. No morphological changes were observed in B-mode throughout the chemotherapy protocol. However, the Doppler velocimetry indices demonstrated statistical differences before (T0) and after (T1) the administration of the drugs. It was concluded that Doppler ultrasound could be used as a complementary method for monitoring the renal response of patients exposed to nephrotoxic drugs and potentially causing renal injury.

As neoplasias mamárias representam o tipo de neoplasma mais frequentemente diagnosticado em fêmeas da espécie canina. Embora a remoção cirúrgica seja o procedimento de eleição para a conduta terapêutica, os protocolos quimioterápicos aparecem como importantes aliados e adjuvantes. Apesar dos grandes avanços ocorridos na área da terapia oncológica, as repercussões sistêmicas destes fármacos ainda impõem importantes limitações ao seu uso. Neste sentido, o desenvolvimento de protocolos terapêuticos cada vez mais direcionados e o monitoramento preventivo dos pacientes representam estratégias importantes para evitar possíveis complicações - dentre elas, a injúria renal aguda (IRA). Rotineiramente, a avaliação ultrassonográfica é utilizada para identificação de variações morfológicas ou metastáticas em órgãos da cavidade abdominal. Atuando de forma complementar à avaliação em modo-B, o mapeamento Doppler mostra-se eficiente no reconhecimento de alterações na hemodinâmica vascular. Portanto, o objetivo do presente estudo foi avaliar a utilização da ultrassonografia modo-B e Doppler como método para identificação de alterações morfológicas e hemodinâmicas renais em cadelas com neoplasias mamárias submetidas a protocolos quimioterápicos adjuvantes que associam a gencitabina à carboplatina. Foram incluídas 13 fêmeas caninas, sem distinção quanto a raça e com idades entre sete e 13 anos. Os animais foram avaliados ultrassonograficamente em dois momentos distintos durante três ciclos quimioterápicos consecutivos: antes (T0) e uma hora e meia após a realização de cada ciclo (T1), totalizando 42 dias. Não foram observadas alterações morfológicas em modo-B ao longo do protocolo quimioterápico. Entretanto, os índices dopplervelocimétricos demonstraram diferenças estatísticas antes (T0) e após (T1) a administração dos fármacos. Concluiu-se que a ultrassonografia Doppler pode ser utilizada como método complementar para o monitoramento da resposta renal de pacientes expostos a fármacos nefrotóxicos e potencialmente causadores de injúrias renais.

Tratamento de reação inflamatória cerebral após Acidente Vascular Encefálico (AVE) e Trauma Cranioencefálico (TCE) em cão / Treatment of inflammatory brain reaction after Brain Vascular Accident (CVA) and Traumatic Brain Injury (TBI) in a dog / Tratamiento de la reacción inflamatoria cerebral después de un Accidente Vascular Cerebral (ACV) y Traumatismo Cerebral (TEC) en un perro

O presente relato de caso tem por objetivo descrever a ocorrência de quadro neurológico tardio, pós-trauma cranioencefálico em um paciente canino, atendido em clínica veterinária particular. O animal foi avaliado clinicamente, com alterações neurológicas intensas de ataxia vestibular, andar compulsivo, paresia, perda de propriocepção nos quatro membros, miose bilateral, anisocoria, entre outros. O diagnóstico foi presuntivo, auxiliado por ressonância magnética, e baseado no histórico detalhado. O tratamento clínico foi determinado empiricamente, a base de dexametasona comercial, associada a metionina, nicotinamida e piridoxina. O paciente apresentou melhora clínica rápida, diminuindo inflamação encefálica e desaparecimento de quadro neurológico.

The present case report aims to describe the occurrence of a late neurological condition, after traumatic brain injury in a canine patient, treated at a private veterinary clinic. The animal was clinically evaluated, with severe neurological alterations of vestibular ataxia, compulsive gait, paresis, loss of proprioception in all four limbs, bilateral miosis, anisocoria, among others. Diagnosis was presumptive, aided by MRI, and based on detailed history. Clinical treatment was empirically determined, based on commercial dexamethasone, associated with methionine, nicotinamide and pyridoxine. The patient showed rapid clinical improvement, with no neurological picture.

El presente reporte de caso tiene como objetivo describir la aparición de una condición neurológica tardía, posterior a un traumatismo craneoencefálico en un paciente canino, atendido en una clínica veterinaria privada. El animal fue evaluado clínicamente, con alteraciones neurológicas severas de ataxia vestibular, marcha compulsiva, paresia, pérdida de propiocepción en las cuatro extremidades, miosis bilateral, anisocoria, entre otras. El diagnóstico fue presuntivo, ayudado por resonancia magnética y basado en una historia clínica detallada. El tratamiento clínico se determinó empíricamente, a base de dexametasona comercial, asociada a metionina, nicotinamida y piridoxina. El paciente presentó una rápida mejoría clínica sin cuadro neurológico.

The use of occlusive dressings: influence on excisional wound healing in animal model

Purpose: To analyze the influence of occlusive dressing on the healing of excisional skin wounds in mice. Methods: Pre-clinical, comparative, and translational study. Mice were divided into three experimental groups: wounds occluded with hydrocolloid (HD) dressings, transparent polyurethane film (TF) dressings, and without occlusion (WO), monitored at three, six and 14 days, with eight animals each. Closure rate, infiltration of neutrophils and macrophages, measurement of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) and, histologically, angiogenesis were evaluated. Results: Wound closure was accelerated in the occlusive groups. There was a decrease in TNF-α levels in the HD group when compared to the WO and TF groups. Neutrophils accumulation decreased in the HD group. Increased dosages of macrophages were evidenced in the HD group, compared to the WO and TF groups. Levels of VEGF were increased in the TF and HD groups. Conclusions: It is suggested that the occlusion of wounds modulates the inflammatory response.

Ehlers-Danlos syndrome in a crossbreed cat / Síndrome de Ehlers-Danlos em um gato mestiço

The Ehlers-Danlos syndrome (EDS) consists of a group of diseases characterized by defective collagen production or failure in its organization, resulting in changes in the strength and extensibility of connective tissue. This report describes the dermatological and histological findings observed in a 3-month-old crossbreed cat with rupture and detachment of skin in the thoracic limb and rupture of the skin in the cervical region. Upon dermatological examination, the cat presented fragile and hyperextensible skin in the cervical region and a skin extensibility index of 21%. Histopathological evaluation of the skin specimens revealed evident disorganization of collagen bundles in dermis and in the Masson's trichrome staining, follicular dysplasia was found. The presumptive diagnosis of EDS was made based on the clinical and histopathological findings. Sanger sequencing did not detect any mutated alleles for the c.3420delG mutation in COL5A1 gene, which was an autosomal dominant mutation previously been associated with Ehlers-Danlos syndrome in cats. The absence of this mutation in the reported cat suggests that other mutation may also be responsible for the development of cutaneous asthenia in this or maybe other genes related to collagen metabolism.

A síndrome de Ehlers-Danlos (EDS) consiste em um conjunto de doenças caracterizadas pela produção deficiente de colágeno ou falha em sua organização, resultando em alterações na resistência e extensibilidade do tecido conjuntivo. Este relato descreve os achados dermatológicos e histológicos observados em um gato mestiço de três meses de idade com ruptura e descolamento de pele do membro torácico e ruptura da pele na região cervical. Ao exame dermatológico, o gato apresentava pele hiper-extensível, fragilizada na região cervical e índice de extensibilidade cutânea de 21%. A avaliação histopatológica das amostras de pele revelou desorganização evidente dos feixes de colágeno na derme e pela coloração com tricrômico de Masson foi encontrada displasia folicular. O diagnóstico presuntivo de EDS foi realizado com base nos achados clínicos e histopatológicos. O sequenciamento de Sanger não detectou nenhum alelo mutado para a mutação c.3420delG no gene COL5A1, que é uma mutação autossômica dominante previamente associada à síndrome de Ehlers-Danlos em gatos. A ausência dessa mutação no gato relatado sugere que outra mutação também pode ser responsável pelo desenvolvimento de astenia cutânea neste gene ou em outro associado ao metabolismo de colágeno.

Effects of systemic inflammation due to hepatic ischemia-reperfusion injury upon lean or obese visceral adipose tissue

Purpose: To evaluate how the induction of liver damage by ischemia and reperfusion affects the adipose tissue of lean and obese mice. Methods: Lean and diet-induced obese mice were subjected to liver ischemia (30 min) followed by 6 h of reperfusion. The vascular stromal fraction of visceral adipose tissue was analyzed by cytometry, and gene expression was evaluated by an Array assay and by RT-qPCR. Intestinal permeability was assessed by oral administration of fluorescein isothiocyanate (FITC)-dextran and endotoxemia by serum endotoxin measurements using a limulus amebocyte lysate assay. Results: It was found that, after liver ischemia and reperfusion, there is an infiltration of neutrophils, monocytes, and lymphocytes, as well as an increase in the gene expression that encode cytokines, chemokines and their receptors in the visceral adipose tissue of lean mice. This inflammatory response was associated with the presence of endotoxemia in lean mice. However, these changes were not observed in the visceral adipose tissue of obese mice. Conclusions: Liver ischemia and reperfusion induce an acute inflammatory response in adipose tissue of lean mice characterized by an intense chemokine induction and leukocyte infiltration; however, inflammatory alterations are already present at baseline in the obese adipose tissue and liver ischemia and reperfusion do not injure further.

Spontaneous and experimental poisoning by nitroxinil at 34% in goats

ABSTRACT: This study describes the epidemiological, clinical, and pathological aspects of spontaneous and experimental poisoning by nitroxinil at 34% concentration in goats. The outbreak occurred on a farm in the municipality of Prata, Paraíba state. Nitroxinil was administered to a herd of 120 goats, of which 18 presented with anorexia, vocalization, abdominal distension, weakness, staggering, and falls. Necropsy of three goats revealed that the main lesion was acute liver injury. Histologically the liver showed centrilobular necrosis associated with hemorrhage and hepatocyte degeneration. In the kidneys, tubular nephrosis with granular cylinder formations was observed. The lungs showed multifocal to coalescent areas of moderate interalveolar edema and vascular congestion. Experimental poisoning was carried out in two goats, with the same medication and doses administered on the farm. The experimental goats showed clinical signs and macroscopic and histological changes similar to the spontaneously poisoned goats. The diagnosis of nitroxinil poisoning was made based on epidemiological, clinical, and pathological data, and confirmed by experimental poisoning. The administration of nitroxinil in high doses, associated with high ambient temperature and physical exercises, can cause poisoning with high lethality in goats.

RESUMO: Este estudo descreve os aspectos epidemiológicos, clínicos e patológicos da intoxicação espontânea e experimental por nitroxinil na concentração de 34% em caprinos. O surto ocorreu em uma fazenda no município de Prata, Paraíba. Nitroxinil foi administrado a um rebanho de 120 cabras, das quais 18 apresentavam anorexia, vocalização, distensão abdominal, fraqueza, cambaleando e quedas. A necropsia de três cabras revelou que a lesão principal era uma lesão hepática aguda. Histologicamente, o fígado apresentava necrose centrolobular associada a hemorragia e degeneração de hepatócitos. Nos rins, nefrose tubular com formações de cilindro granular foi observada. Os pulmões apresentavam áreas multifocais a coalescentes de edema interalveolar moderado e congestão vascular. A intoxicação experimental foi realizada em duas cabras, com a mesma medicação e doses administradas na fazenda. As cabras experimentais apresentaram sinais clínicos e alterações macroscópicas e histológicas semelhantes às cabras intoxicadas espontaneamente. O diagnóstico de intoxicação por nitroxinil foi feito com base em dados epidemiológicos, clínicos e patológicos, e confirmado por intoxicação experimental. A administração de nitroxinil em altas doses, associada à alta temperatura ambiente e exercícios físicos, pode causar intoxicação com alta letalidade em caprinos.

Spontaneous and experimental poisoning by nitroxinil at 34% in goats / Intoxicação espontânea e experimental por nitroxinil na concentração de 34% em caprinos

This study describes the epidemiological, clinical, and pathological aspects of spontaneous and experimental poisoning by nitroxinil at 34% concentration in goats. The outbreak occurred on a farm in the municipality of Prata, Paraíba state. Nitroxinil was administered to a herd of 120 goats, of which 18 presented with anorexia, vocalization, abdominal distension, weakness, staggering, and falls. Necropsy of three goats revealed that the main lesion was acute liver injury. Histologically the liver showed centrilobular necrosis associated with hemorrhage and hepatocyte degeneration. In the kidneys, tubular nephrosis with granular cylinder formations was observed. The lungs showed multifocal to coalescent areas of moderate interalveolar edema and vascular congestion. Experimental poisoning was carried out in two goats, with the same medication and doses administered on the farm. The experimental goats showed clinical signs and macroscopic and histological changes similar to the spontaneously poisoned goats. The diagnosis of nitroxinil poisoning was made based on epidemiological, clinical, and pathological data, and confirmed by experimental poisoning. The administration of nitroxinil in high doses, associated with high ambient temperature and physical exercises, can cause poisoning with high lethality in goats.(AU)

Este estudo descreve os aspectos epidemiológicos, clínicos e patológicos da intoxicação espontânea e experimental por nitroxinil na concentração de 34% em caprinos. O surto ocorreu em uma fazenda no município de Prata, Paraíba. Nitroxinil foi administrado a um rebanho de 120 cabras, das quais 18 apresentavam anorexia, vocalização, distensão abdominal, fraqueza, cambaleando e quedas. A necropsia de três cabras revelou que a lesão principal era uma lesão hepática aguda. Histologicamente, o fígado apresentava necrose centrolobular associada a hemorragia e degeneração de hepatócitos. Nos rins, nefrose tubular com formações de cilindro granular foi observada. Os pulmões apresentavam áreas multifocais a coalescentes de edema interalveolar moderado e congestão vascular. A intoxicação experimental foi realizada em duas cabras, com a mesma medicação e doses administradas na fazenda. As cabras experimentais apresentaram sinais clínicos e alterações macroscópicas e histológicas semelhantes às cabras intoxicadas espontaneamente. O diagnóstico de intoxicação por nitroxinil foi feito com base em dados epidemiológicos, clínicos e patológicos, e confirmado por intoxicação experimental. A administração de nitroxinil em altas doses, associada à alta temperatura ambiente e exercícios físicos, pode causar intoxicação com alta letalidade em caprinos.(AU)

Spontaneous and experimental poisoning by nitroxinil at 34% in goats / Intoxicação espontânea e experimental por nitroxinil na concentração de 34% em caprinos

This study describes the epidemiological, clinical, and pathological aspects of spontaneous and experimental poisoning by nitroxinil at 34% concentration in goats. The outbreak occurred on a farm in the municipality of Prata, Paraíba state. Nitroxinil was administered to a herd of 120 goats, of which 18 presented with anorexia, vocalization, abdominal distension, weakness, staggering, and falls. Necropsy of three goats revealed that the main lesion was acute liver injury. Histologically the liver showed centrilobular necrosis associated with hemorrhage and hepatocyte degeneration. In the kidneys, tubular nephrosis with granular cylinder formations was observed. The lungs showed multifocal to coalescent areas of moderate interalveolar edema and vascular congestion. Experimental poisoning was carried out in two goats, with the same medication and doses administered on the farm. The experimental goats showed clinical signs and macroscopic and histological changes similar to the spontaneously poisoned goats. The diagnosis of nitroxinil poisoning was made based on epidemiological, clinical, and pathological data, and confirmed by experimental poisoning. The administration of nitroxinil in high doses, associated with high ambient temperature and physical exercises, can cause poisoning with high lethality in goats.(AU)

Este estudo descreve os aspectos epidemiológicos, clínicos e patológicos da intoxicação espontânea e experimental por nitroxinil na concentração de 34% em caprinos. O surto ocorreu em uma fazenda no município de Prata, Paraíba. Nitroxinil foi administrado a um rebanho de 120 cabras, das quais 18 apresentavam anorexia, vocalização, distensão abdominal, fraqueza, cambaleando e quedas. A necropsia de três cabras revelou que a lesão principal era uma lesão hepática aguda. Histologicamente, o fígado apresentava necrose centrolobular associada a hemorragia e degeneração de hepatócitos. Nos rins, nefrose tubular com formações de cilindro granular foi observada. Os pulmões apresentavam áreas multifocais a coalescentes de edema interalveolar moderado e congestão vascular. A intoxicação experimental foi realizada em duas cabras, com a mesma medicação e doses administradas na fazenda. As cabras experimentais apresentaram sinais clínicos e alterações macroscópicas e histológicas semelhantes às cabras intoxicadas espontaneamente. O diagnóstico de intoxicação por nitroxinil foi feito com base em dados epidemiológicos, clínicos e patológicos, e confirmado por intoxicação experimental. A administração de nitroxinil em altas doses, associada à alta temperatura ambiente e exercícios físicos, pode causar intoxicação com alta letalidade em caprinos.(AU)

Ischemic perconditioning on mesenteric ischemia/reperfusion injury in rats

ABSTRACT Purpose: To evaluate if the perconditioning affects the antioxidant capacity in mesenteric ischemia and reperfusion injury. Methods: Twenty-one Wistar rats were assigned into three groups, as follows: Sham, IR and rPER. The animals were subjected to mesenteric ischemia for 30 min. rPER consisted of three cycles of 5-min hindlimb ischemia followed by 5 min hindlimb perfusion at the same time to mesenteric ischemic period. After 5 minutes, blood and 5 cm of terminal ileum were harvested for thiobarbituric acid reactive substances (TBARS) and Trolox equivalent antioxidant capacity (TEAC) measurement. Results: rPER technique was able to reduce intestinal tissue TBARS levels (p<0.0001), but no statistic difference was observed in blood levels between groups, although it was verified similar results in rPER and Sham group. rPER technique also enhanced TEAC levels in both blood (p = 0.0314) and intestinal tissue (p = 0.0139), compared to IR group. Conclusions: rPER appears as the most promising technique to avoid IR injury. This technique reduced TBARS levels in blood and intestinal tissue and promoted the maintenance of antioxidant defense in mesenteric acute injury.

Hydrogen-rich saline alleviates early brain injury through regulating of ER stress and autophagy after experimental subarachnoid hemorrhage

ABSTRACT Purpose: Subarachnoid hemorrhage (SAH) is a common complication of cerebral vascular disease. Hydrogen has been reported to alleviate early brain injury (EBI) through oxidative stress injury, reactive oxygen species (ROS), and autophagy. Autophagy is a programmed cell death mechanism that plays a vital role in neuronal cell death after SAH. However, the precise role of autophagy in hydrogen-mediated neuroprotection following SAH has not been confirmed. Methods: In the present study, the objective was to investigate the neuroprotective effects and potential molecular mechanisms of hydrogen-rich saline in SAH-induced EBI by regulating neural autophagy in the C57BL/6 mice model. Mortality, neurological score, brain water content, ROS, malondialdehyde (MDA), and neuronal death were evaluated. Results: The results show that hydrogen-rich saline treatment markedly increased the survival rate and neurological score, increased neuron survival, downregulated the autophagy protein expression of Beclin-1 and LC3, and endoplasmic reticulum (ER) stress. That indicates that hydrogen-rich saline-mediated inhibition of autophagy and ER stress ameliorate neuronal death after SAH. The neuroprotective capacity of hydrogen-rich saline is partly dependent on the ROS/Nrf2/heme oxygenase-1 (HO-1) signaling pathway. Conclusions: The results of this study demonstrate that hydrogen-rich saline improves neurological outcomes in mice and reduces neuronal death by protecting against neural autophagy and ER stress.

The effect of dexmedetomidine on gastric ischemia reperfusion injury in rats: biochemical and histopathological evaluation

Purpose: To evaluate the protective effect of dexmedetomidine on gastric injury induced by ischemia reperfusion (I/R) in rats. Methods: A total of 18 male albino Wistar rats were divided groups as: gastric ischemia reperfusion (GIR), gastric ischemia reperfusion and 50 g/kg dexmedetomidine (DGIR) and sham operation (HG) group. After the third hour of reperfusion, the biochemical and histopathological examinations were performed on the removed stomach tissue. Results: Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were found to be significantly higher in GIR compared to HG (p 0.05). A statistically significant decrease was observed at the DGIR compared to the GIR for oxidants levels. Total glutathione (tGSH) and superoxide dismutase (SOD) levels were statistically significantly decreased at the GIR, and antioxidants levels were found to be significantly higher in the DGIR (p 0.05) There was no significant difference between HG and DGIR in terms of SOD (p = 0.097). The DGIRs epitheliums, glands and vascular structures were close to normal histological formation. Conclusions: Dexmedetomidine is found to prevent oxidative damage on the stomach by increasing the antioxidant effect. These results indicate that dexmedetomidine may be useful in the treatment of ischemia-reperfusion-related gastric damage.(AU)

The protective effect of Ganoderma lucidum on testicular torsion/detorsion-induced ischemia-reperfusion (I/R) injury

Purpose To investigate the protective effect of Ganoderma lucidum on testicular torsion/detorsion (T/D)-induced ischemia-reperfusion (I/R) injury. Methods Thirty male Wistar albino rats were randomly categorized into 3 groups: Group 1: sham, Group 2 ( T/D): 2,5 hours of ischemia and 7 days of reperfusion, Group 3 (T/D+ G. lucidum ): 2,5 hours of ischemia and 7 days of reperfusion and 7 days of 20 mg/kg via gastric gavage G. lucidum polysaccharides per day. Biochemical assays of Malondialdehyde (MDA), superoxide dismutase (SOD), Catalase (CAT), Glutathione (GSH) levels , histopathology and expression levels of VEGF and Bcl-2 with immunohistochemical methods were examined in testicular tissue. Results G. lucidum treatment was found to have prevented the T/D-induced I/R injury by decreasing MDA levels of the testis. SOD, CAT and GSH activities were decreased in group 2, while they were increased in group 3 (p<0.001) and significant improvement in the tube diameter was observed in group 3. Bcl-2-positive germinal cells were lowered in group 3 compared to the group 2. VEGF expression showed an increase in group 2, whereas it decreased in group 3. Conclusion The antioxidant G. lucidum is thought to induce angiogenesis by reducing the apoptotic effect in testicular torsion-detorsion.(AU)

Effects of oxidative stress on liver, brain and spinal cord of rats using L-NAME and treated with hydroxyurea: a model of sickle cell complication

Purpose: To analyze the serum levels of nitric oxide and correlate them with the levels of thiobarbituric acid reactive substances (TBARS) in liver, brain and spinal cord of animals using L-NAME and treated with hydroxyurea. Methods: Eighteen male albino Wistar rats were divided into three groups. NG-nitro-L-arginine methyl ester (L-NAME) was intraperitoneally administered to induce oxidative stress. TBARS and plasma nitric oxide levels were analyzed in all groups. Histopathology of the liver and vascular tissue was performed. Results: Statistically significant differences were seen in liver, brain and spinal cord TBARS levels. Conclusions: Following the use of L-NAME, hepatic tissue increased the number of Kupffer cells as oxidative stress and inflammatory response increased. The use of L-NAME caused an increase in lipid peroxidation products and, consequently, in oxidative stress in animals. Hydroxyurea doses of 35 mg / kg / day reduced TBARS values in liver, brain and spinal cord.(AU)

Dystrophic mineralization in uremic dogs: an update

ABSTRACT: Pathological mineralization is the abnormal deposition of minerals in body tissues, previously injured or not. In these lesions, in addition to calcium, other minerals can be found at lower concentrations. Classically, mineralization is divided into two types: dystrophic and metastatic. However, currently, there is no consensus among researchers on the type of mineralization that occurs in uremic dogs. The objective of this study was to elucidate the type of pathological mineralization that occurs in dogs with uremic syndrome through the correlation of biochemical examinations with gross and histopathological changes, given the existence of controversial information on this theme in the specialized literature. The Shapiro-Wilk, DAgostino and Pearson tests were used to evaluate data normality distribution, and analysis of variance (ANOVA) was applied to compare the data between more than two groups. Additionally, the Dunnetts multiple comparison test was used in the comparison between the Control Group (CG) and the Experimental Groups (G1, G2, and G3). Serum levels of urea, creatinine, total and ionized calcium, phosphorus, calcium-phosphorus product (CPP), parathyroid hormone (PTH), and albumin of 40 azotemic dogs with chronic kidney disease (CKD) were evaluated. Dogs were categorized by degree of azotemia (mild, moderate, and severe). Ionized hypocalcemia was observed in 97.5% (39/40) of the dogs, and no animals presented ionized hypercalcemia. Hyperphosphatemia was frequent (62.5%), especially in dogs with severe azotemia. PTH concentration increased with progression of azotemia, and high PTH levels were verified in 100% of the dogs with severe azotemia. CPP >60mg2/dl2 was observed in 75% (30/40) of the dogs. Of the 29 dogs that died during the study period, 16 were necropsied. Soft tissue mineralization was observed in 93.7% (15/16) of these dogs at gross and histopathological evaluation (HE and Von Kossa), regardless of the degree of azotemia, in nine organs/tissues: kidneys (75%), lungs (50%), stomach (31.2%), heart (25%), larynx (25%), intercostal muscles (25%), aorta (6.2%), intestines (6.2%), and tongue (6.2%). In one animal, the serosa of all segments of the small intestine showed whitish, rough, irregular, multifocal plaques of varying sizes, confirmed by histopathology as dystrophic mineralization of the longitudinal outer muscular layer, which presented necrosis of coagulation and of the intestinal serosa. This intestinal lesion has not been described in dogs with uremic syndrome to date. In conclusion, the laboratory and histopathologic data previously described, especially regarding tissue and vascular mineralization, which occur in association with previous degenerative/necrotic lesions in the absence of hypercalcemia in dogs with CKD, assist with clarifying inconsistencies found in the existing literature. Therefore, conceptually, mineralization that occurs in uremic dogs should be considered dystrophic.

RESUMO: Mineralização patológica é a deposição anormal de minerais em tecidos previamente lesados ou não. Nessas lesões, além do cálcio, outros minerais podem ser encontrados em concentrações inferiores. Classicamente, as mineralizações são divididas em dois tipos: distrófica e metastática. Contudo, atualmente, ainda não há consenso entre os pesquisadores sobre o tipo de mineralização que ocorre em cães urêmicos. Objetivou-se com esse estudo elucidar o tipo de mineralização patológica que ocorre em cães com síndrome urêmica através da correlação de exames bioquímicos com alterações macroscópicas e histopatológicas, visto a existência de informações controversas na literatura especializada. Os dados obtidos foram submetidos ao teste de Shapiro-Wilk e teste de DAgostino e Pearson para avaliação da normalidade da distribuição e para comparação de dados em mais de dois grupos foi utilizado o teste ANOVA. Adicionalmente, o teste de comparações múltiplas de Dunnett permitiu a comparação entre o grupo controle (GC) com os demais grupos (G1, G2 e G3). Foram avaliados os níveis séricos de ureia, creatinina, cálcio total e ionizado, fósforo, produto cálcio-fósforo (PCF), PTH e albumina de 40 cães azotêmicos com doença renal crônica (DRC). Os cães foram classificados quanto ao grau de azotemia (leve, moderada e severa). Verificou-se hipocalcemia ionizada em 97,5% (39/40) dos cães e, em nenhum animal houve hipercalcemia ionizada. Hiperfosfatemia foi frequente (62,5%), principalmente em cães com azotemia severa. A concentração do PTH aumentou conforme a progressão da azotemia, encontrando-se elevada em 100% dos cães com azotemia severa. Em 75% (30/40) dos cães o PCF foi superior a 60mg2/dl2. Durante o estudo, 29 cães morreram, sendo 16 desses necropsiados. Em 93,7% (15/16) desses cães observou-se mineralização de tecidos moles, durante a avaliação macroscópica e histopatológica (HE e Von Kossa), independentemente do grau de azotemia, em nove órgãos/tecidos: rins (75%), pulmões (50%), estômago (31,2%), coração (25%), laringe (25%), músculos intercostais (25%), aorta (6,2%), intestino (6,2%) e língua (6,2%). Adicionalmente, em um animal verificou-se na serosa de todos os segmentos do intestino delgado placas multifocais brancacentas, rugosas, irregulares de tamanhos variados, cuja histopatologia confirmou tratar-se de mineralização distrófica da camada longitudinal muscular externa que apresentava necrose de coagulação e da serosa intestinal. Essa lesão intestinal nunca havia sido descrita em cães com síndrome urêmica. Em suma, os dados laboratoriais e histopatológicos aqui descritos, sobretudo, no que se refere à mineralização tecidual e vascular, que ocorrem relacionadas a lesões degenerativo-necróticas prévias, na ausência de hipercalcemia, em cães com DRC, ajudam a esclarecer as incongruências existentes na literatura. Por conseguinte, conceitualmente, as mineralizações que ocorrem em cães urêmicos devem ser consideradas distróficas.

Dystrophic mineralization in uremic dogs: an update / Mineralização distrófica em cães urêmicos: uma atualização

Pathological mineralization is the abnormal deposition of minerals in body tissues, previously injured or not. In these lesions, in addition to calcium, other minerals can be found at lower concentrations. Classically, mineralization is divided into two types: dystrophic and metastatic. However, currently, there is no consensus among researchers on the type of mineralization that occurs in uremic dogs. The objective of this study was to elucidate the type of pathological mineralization that occurs in dogs with uremic syndrome through the correlation of biochemical examinations with gross and histopathological changes, given the existence of controversial information on this theme in the specialized literature. The Shapiro-Wilk, D'Agostino and Pearson tests were used to evaluate data normality distribution, and analysis of variance (ANOVA) was applied to compare the data between more than two groups. Additionally, the Dunnett's multiple comparison test was used in the comparison between the Control Group (CG) and the Experimental Groups (G1, G2, and G3). Serum levels of urea, creatinine, total and ionized calcium, phosphorus, calcium-phosphorus product (CPP), parathyroid hormone (PTH), and albumin of 40 azotemic dogs with chronic kidney disease (CKD) were evaluated. Dogs were categorized by degree of azotemia (mild, moderate, and severe). Ionized hypocalcemia was observed in 97.5% (39/40) of the dogs, and no animals presented ionized hypercalcemia. Hyperphosphatemia was frequent (62.5%), especially in dogs with severe azotemia. PTH concentration increased with progression of azotemia, and high PTH levels were verified in 100% of the dogs with severe azotemia. CPP >60mg2/dl2 was observed in 75% (30/40) of the dogs. Of the 29 dogs that died during the study period, 16 were necropsied. Soft tissue mineralization was observed in 93.7% (15/16) of these dogs at gross and histopathological evaluation (HE and Von Kossa), regardless of the degree of azotemia, in nine organs/tissues: kidneys (75%), lungs (50%), stomach (31.2%), heart (25%), larynx (25%), intercostal muscles (25%), aorta (6.2%), intestines (6.2%), and tongue (6.2%). In one animal, the serosa of all segments of the small intestine showed whitish, rough, irregular, multifocal plaques of varying sizes, confirmed by histopathology as dystrophic mineralization of the longitudinal outer muscular layer, which presented necrosis of coagulation and of the intestinal serosa. This intestinal lesion has not been described in dogs with uremic syndrome to date. In conclusion, the laboratory and histopathologic data previously described, especially regarding tissue and vascular mineralization, which occur in association with previous degenerative/necrotic lesions in the absence of hypercalcemia in dogs with CKD, assist with clarifying inconsistencies found in the existing literature. Therefore, conceptually, mineralization that occurs in uremic dogs should be considered dystrophic.(AU)

Mineralização patológica é a deposição anormal de minerais em tecidos previamente lesados ou não. Nessas lesões, além do cálcio, outros minerais podem ser encontrados em concentrações inferiores. Classicamente, as mineralizações são divididas em dois tipos: distrófica e metastática. Contudo, atualmente, ainda não há consenso entre os pesquisadores sobre o tipo de mineralização que ocorre em cães urêmicos. Objetivou-se com esse estudo elucidar o tipo de mineralização patológica que ocorre em cães com síndrome urêmica através da correlação de exames bioquímicos com alterações macroscópicas e histopatológicas, visto a existência de informações controversas na literatura especializada. Os dados obtidos foram submetidos ao teste de Shapiro-Wilk e teste de D'Agostino e Pearson para avaliação da normalidade da distribuição e para comparação de dados em mais de dois grupos foi utilizado o teste ANOVA. Adicionalmente, o teste de comparações múltiplas de Dunnett permitiu a comparação entre o grupo controle (GC) com os demais grupos (G1, G2 e G3). Foram avaliados os níveis séricos de ureia, creatinina, cálcio total e ionizado, fósforo, produto cálcio-fósforo (PCF), PTH e albumina de 40 cães azotêmicos com doença renal crônica (DRC). Os cães foram classificados quanto ao grau de azotemia (leve, moderada e severa). Verificou-se hipocalcemia ionizada em 97,5% (39/40) dos cães e, em nenhum animal houve hipercalcemia ionizada. Hiperfosfatemia foi frequente (62,5%), principalmente em cães com azotemia severa. A concentração do PTH aumentou conforme a progressão da azotemia, encontrando-se elevada em 100% dos cães com azotemia severa. Em 75% (30/40) dos cães o PCF foi superior a 60mg2/dl2. Durante o estudo, 29 cães morreram, sendo 16 desses necropsiados. Em 93,7% (15/16) desses cães observou-se mineralização de tecidos moles, durante a avaliação macroscópica e histopatológica (HE e Von Kossa), independentemente do grau de azotemia, em nove órgãos/tecidos: rins (75%), pulmões (50%), estômago (31,2%), coração (25%), laringe (25%), músculos intercostais (25%), aorta (6,2%), intestino (6,2%) e língua (6,2%). Adicionalmente, em um animal verificou-se na serosa de todos os segmentos do intestino delgado placas multifocais brancacentas, rugosas, irregulares de tamanhos variados, cuja histopatologia confirmou tratar-se de mineralização distrófica da camada longitudinal muscular externa que apresentava necrose de coagulação e da serosa intestinal. Essa lesão intestinal nunca havia sido descrita em cães com síndrome urêmica. Em suma, os dados laboratoriais e histopatológicos aqui descritos, sobretudo, no que se refere à mineralização tecidual e vascular, que ocorrem relacionadas a lesões degenerativo-necróticas prévias, na ausência de hipercalcemia, em cães com DRC, ajudam a esclarecer as incongruências existentes na literatura. Por conseguinte, conceitualmente, as mineralizações que ocorrem em cães urêmicos devem ser consideradas distróficas.(AU)

Dystrophic mineralization in uremic dogs: an update / Mineralização distrófica em cães urêmicos: uma atualização

Pathological mineralization is the abnormal deposition of minerals in body tissues, previously injured or not. In these lesions, in addition to calcium, other minerals can be found at lower concentrations. Classically, mineralization is divided into two types: dystrophic and metastatic. However, currently, there is no consensus among researchers on the type of mineralization that occurs in uremic dogs. The objective of this study was to elucidate the type of pathological mineralization that occurs in dogs with uremic syndrome through the correlation of biochemical examinations with gross and histopathological changes, given the existence of controversial information on this theme in the specialized literature. The Shapiro-Wilk, D'Agostino and Pearson tests were used to evaluate data normality distribution, and analysis of variance (ANOVA) was applied to compare the data between more than two groups. Additionally, the Dunnett's multiple comparison test was used in the comparison between the Control Group (CG) and the Experimental Groups (G1, G2, and G3). Serum levels of urea, creatinine, total and ionized calcium, phosphorus, calcium-phosphorus product (CPP), parathyroid hormone (PTH), and albumin of 40 azotemic dogs with chronic kidney disease (CKD) were evaluated. Dogs were categorized by degree of azotemia (mild, moderate, and severe). Ionized hypocalcemia was observed in 97.5% (39/40) of the dogs, and no animals presented ionized hypercalcemia. Hyperphosphatemia was frequent (62.5%), especially in dogs with severe azotemia. PTH concentration increased with progression of azotemia, and high PTH levels were verified in 100% of the dogs with severe azotemia. CPP >60mg2/dl2 was observed in 75% (30/40) of the dogs. Of the 29 dogs that died during the study period, 16 were necropsied. Soft tissue mineralization was observed in 93.7% (15/16) of these dogs at gross and histopathological evaluation (HE and Von Kossa), regardless of the degree of azotemia, in nine organs/tissues: kidneys (75%), lungs (50%), stomach (31.2%), heart (25%), larynx (25%), intercostal muscles (25%), aorta (6.2%), intestines (6.2%), and tongue (6.2%). In one animal, the serosa of all segments of the small intestine showed whitish, rough, irregular, multifocal plaques of varying sizes, confirmed by histopathology as dystrophic mineralization of the longitudinal outer muscular layer, which presented necrosis of coagulation and of the intestinal serosa. This intestinal lesion has not been described in dogs with uremic syndrome to date. In conclusion, the laboratory and histopathologic data previously described, especially regarding tissue and vascular mineralization, which occur in association with previous degenerative/necrotic lesions in the absence of hypercalcemia in dogs with CKD, assist with clarifying inconsistencies found in the existing literature. Therefore, conceptually, mineralization that occurs in uremic dogs should be considered dystrophic.(AU)

Mineralização patológica é a deposição anormal de minerais em tecidos previamente lesados ou não. Nessas lesões, além do cálcio, outros minerais podem ser encontrados em concentrações inferiores. Classicamente, as mineralizações são divididas em dois tipos: distrófica e metastática. Contudo, atualmente, ainda não há consenso entre os pesquisadores sobre o tipo de mineralização que ocorre em cães urêmicos. Objetivou-se com esse estudo elucidar o tipo de mineralização patológica que ocorre em cães com síndrome urêmica através da correlação de exames bioquímicos com alterações macroscópicas e histopatológicas, visto a existência de informações controversas na literatura especializada. Os dados obtidos foram submetidos ao teste de Shapiro-Wilk e teste de D'Agostino e Pearson para avaliação da normalidade da distribuição e para comparação de dados em mais de dois grupos foi utilizado o teste ANOVA. Adicionalmente, o teste de comparações múltiplas de Dunnett permitiu a comparação entre o grupo controle (GC) com os demais grupos (G1, G2 e G3). Foram avaliados os níveis séricos de ureia, creatinina, cálcio total e ionizado, fósforo, produto cálcio-fósforo (PCF), PTH e albumina de 40 cães azotêmicos com doença renal crônica (DRC). Os cães foram classificados quanto ao grau de azotemia (leve, moderada e severa). Verificou-se hipocalcemia ionizada em 97,5% (39/40) dos cães e, em nenhum animal houve hipercalcemia ionizada. Hiperfosfatemia foi frequente (62,5%), principalmente em cães com azotemia severa. A concentração do PTH aumentou conforme a progressão da azotemia, encontrando-se elevada em 100% dos cães com azotemia severa. Em 75% (30/40) dos cães o PCF foi superior a 60mg2/dl2. Durante o estudo, 29 cães morreram, sendo 16 desses necropsiados. Em 93,7% (15/16) desses cães observou-se mineralização de tecidos moles, durante a avaliação macroscópica e histopatológica (HE e Von Kossa), independentemente do grau de azotemia, em nove órgãos/tecidos: rins (75%), pulmões (50%), estômago (31,2%), coração (25%), laringe (25%), músculos intercostais (25%), aorta (6,2%), intestino (6,2%) e língua (6,2%). Adicionalmente, em um animal verificou-se na serosa de todos os segmentos do intestino delgado placas multifocais brancacentas, rugosas, irregulares de tamanhos variados, cuja histopatologia confirmou tratar-se de mineralização distrófica da camada longitudinal muscular externa que apresentava necrose de coagulação e da serosa intestinal. Essa lesão intestinal nunca havia sido descrita em cães com síndrome urêmica. Em suma, os dados laboratoriais e histopatológicos aqui descritos, sobretudo, no que se refere à mineralização tecidual e vascular, que ocorrem relacionadas a lesões degenerativo-necróticas prévias, na ausência de hipercalcemia, em cães com DRC, ajudam a esclarecer as incongruências existentes na literatura. Por conseguinte, conceitualmente, as mineralizações que ocorrem em cães urêmicos devem ser consideradas distróficas.(AU)