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Hypertrophic cardiomyopathy (HCM) is a common cardiovascular condition in cats, affecting yth males and females of all ages. Some breeds, such as Ragdolls and Maine Coons, can develop HCM at a young age. The disease has a wide range of progression and severity, characterized by various pathological changes in the heart, including arteritis, fibrous tissue deposition, and myocardial cell hypertrophy. Left ventricular hypertrophy, which can restrict blood flow, is a common feature of HCM. The disease may persist into old age and eventually lead to heart failure and increased diastolic pressure. The basis of HCM in cats is thought to be genetic, although the exact mechanisms are not fully understood. Mutations in sarcomeric proteins, in particular myosin-binding protein C (MYBPC3), have been identified in cats with HCM. Two specific mutations, MYBPC3 [R818W] and MYBPC3 [A31P], have been classified as 'pathogenic'. Other variants in genes such as MYBPC3, TNNT2, ALMS1, and MYH7 are also associated with HCM. However, there are cases where cats without known genetic mutations still develop HCM, suggesting the presence of unknown genetic factors contributing to the disease. This work aims to summarise the new knowledge of HCM in cats and the alterations in cardiac tissue as a result of genetic variants.
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Excessive consumption of food rich in saturated fatty acids and carbohydrates can lead to metabolic disturbances and cardiovascular disease. Hyperlipidemia is a significant risk factor for acute cardiac events due to its association with oxidative stress. This leads to arterial wall remodeling, including an increase in the thickness of the intima media complex (IMT), and endothelial dysfunction leading to plaque formation. The decreased nitric oxide synthesis and accumulation of lipids in the wall result in a reduction in the vasodilating potential of the vessel. This study aimed to establish a clear relationship between markers of endothelial dysfunction and the activity of repair enzymes in cardiac tissue from a pig model of early atherosclerosis. The study was conducted on 28 female Polish Landrace pigs, weighing 40 kg (approximately 3.5 months old), which were divided into three groups. The control group (n = 11) was fed a standard, commercial, balanced diet (BDG) for 12 months. The second group (n = 9) was fed an unbalanced, high-calorie Western-type diet (UDG). The third group (n = 8) was fed a Western-type diet for nine months and then switched to a standard, balanced diet (regression group, RG). Control examinations, including blood and urine sampling, were conducted every three months under identical conditions with food restriction for 12 h and water restriction for four hours before general anesthesia. The study analyzed markers of oxidative stress formed during lipid peroxidation processes, including etheno DNA adducts, ADMA, and NEFA. These markers play a crucial role in reactive oxygen species analysis in ischemia-reperfusion and atherosclerosis in mammalian tissue. Essential genes involved in oxidative-stress-induced DNA demethylation like OGG1 (8-oxoguanine DNA glycosylase), MPG (N-Methylpurine DNA Glycosylase), TDG (Thymine-DNA glycosylase), APEX (apurinic/apirymidinic endodeoxyribonuclease 1), PTGS2 (prostaglandin-endoperoxide synthase 2), and ALOX (Arachidonate Lipoxygenase) were measured using the Real-Time RT-PCR method. The data suggest that high oxidative stress, as indicated by TBARS levels, is associated with high levels of DNA repair enzymes and depends on the expression of genes involved in the repair pathway. In all analyzed groups of heart tissue homogenates, the highest enzyme activity and gene expression values were observed for the OGG1 protein recognizing the modified 8oxoG. Conclusion: With the long-term use of an unbalanced diet, the levels of all DNA repair genes are increased, especially (significantly) Apex, Alox, and Ptgs, which strongly supports the hypothesis that an unbalanced diet induces oxidative stress that deregulates DNA repair mechanisms and may contribute to genome instability and tissue damage.
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Aterosclerose , DNA Glicosilases , Timina DNA Glicosilase , Feminino , Animais , Suínos , DNA Glicosilases/genética , DNA Glicosilases/metabolismo , Reparo do DNA , Aterosclerose/genética , Aterosclerose/metabolismo , Estresse Oxidativo , Adutos de DNA , Timina DNA Glicosilase/metabolismo , Dano ao DNA , Mamíferos/metabolismoRESUMO
Despite advances in the management of iron deficiency in heart failure (HF), the mechanisms underlying the effects of treatment remain to be established. Iron distribution and metabolism in HF pathogenesis need to be clarified. We used a porcine tachycardia-induced cardiomyopathy model to find out how HF development influences hepatic and myocardial iron storing, focusing on ferritin, the main iron storage protein. We found that cumulative liver congestion (due to the decrease of heart function) overwhelms its capacity to recycle iron from erythrocytes. As a consequence, iron is trapped in the liver as poorly mobilized hemosiderin. What is more, the ferritin-bound Fe3+ (reflecting bioavailable iron stores), and assembled ferritin (reflecting ability to store iron) are decreased in HF progression in the liver. We demonstrate that while HF pigs show iron deficiency indices, erythropoiesis is enhanced. Renin-angiotensin-aldosterone system activation and hepatic hepcidin suppression might indicate stress erythropoiesisinduced in HF. Furthermore, assembled ferritin increases but ferritin-bound Fe3+ is reduced in myocardium, indicating that a failing heart increases the iron storage reserve but iron deficiency leads to a drop in myocardial iron stores. Together, HF in pigs leads to down-regulated iron bioavailability and reduced hepatic iron storage making iron unavailable for systemic/cardiac needs.
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Insuficiência Cardíaca/metabolismo , Hemossiderina/metabolismo , Fígado/metabolismo , Taquicardia/complicações , Animais , Modelos Animais de Doenças , Ferritinas/metabolismo , Humanos , Ferro/metabolismo , Masculino , Sistema Renina-Angiotensina , Suínos , Taquicardia/etiologia , Taquicardia/metabolismoRESUMO
OBJECTIVE: The role of inhaled nitric oxide in the treatment of shock remains controversial and further translational research is needed. Long-term observation studies using a model of endotoxin-induced shock to assess the effect of inhaled nitric oxide on platelet aggregation have not yet been reported. APPROACH AND RESULTS: The tests were carried out in an animal model of shock in two 10-h periods. During the first 10 h, endotoxin was infused and the inhibition of platelet aggregation was evaluated; following the termination of endotoxin infusion, the restoration of platelet aggregation was assessed for 10 h. A total of 30 pigs were used (NO group, N = 14; control, N = 16). In the NO group, nitric oxide inhalation (30 ppm) was started 3 h after endotoxin infusion and continued until the end of the study. Treatment with NO selectively decreased pulmonary artery pressure at 4 (p = 0.002) and 8 h (p = 0.05) of the experiment as compared to the control. Endotoxin significantly reduced platelet aggregation, as indicated by the decreased activity of platelet receptors: ASPI, ADP, collagen, and TRAP during the experiment (p < 0.001). Endotoxin had no significant effect on changes in the response of the receptor after ristocetin stimulation. After stopping endotoxin infusion, a significant restoration of receptor activity was observed for collagen and TRAP, while ASPI and ADP remained partially depressed. Inhaled nitric oxide did not cause additional inhibition of platelet aggregation, either during or after endotoxin challenge. CONCLUSIONS: A profound reduction in platelet aggregation was observed during endotoxic shock. After stopping endotoxin infusion a restoration of platelet receptor activity was seen. The inhibition of platelet aggregation induced by endotoxin infusion was not intensified by nitric oxide, indicating there was no harmful effect of inhaled nitric oxide on platelet aggregation.
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Plaquetas/metabolismo , Óxido Nítrico/uso terapêutico , Agregação Plaquetária/efeitos dos fármacos , Choque Séptico/tratamento farmacológico , Administração por Inalação , Animais , Endotoxinas , Hidrocortisona/uso terapêutico , Óxido Nítrico/administração & dosagem , Pressão Propulsora Pulmonar/efeitos dos fármacos , Choque Séptico/induzido quimicamente , Choque Séptico/metabolismo , Suínos , Vasodilatadores/administração & dosagem , Vasodilatadores/uso terapêuticoRESUMO
Liposomal technologies are used in order to improve the effectiveness of current therapies or to reduce their negative side effects. However, the liposome-erythrocyte interaction during the intravenous administration of liposomal drug formulations may result in changes within the red blood cells (RBCs). In this study, it was shown that phosphatidylcholine-composed liposomal formulations of Photolon, used as a drug model, significantly influences the transmembrane potential, stiffness, as well as the shape of RBCs. These changes caused decreasing the number of stomatocytes and irregular shapes proportion within the cells exposed to liposomes. Thus, the reduction of anisocytosis was observed. Therefore, some nanodrugs in phosphatidylcholine liposomal formulation may have a beneficial effect on the survival time of erythrocytes.
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Composição de Medicamentos/métodos , Eritrócitos/citologia , Hemólise/efeitos dos fármacos , Lipossomos/química , Potenciais da Membrana , Porfirinas/farmacologia , Radiossensibilizantes/farmacologia , Animais , Forma Celular , Clorofilídeos , Eritrócitos/efeitos dos fármacos , Eritrócitos/fisiologia , Feminino , Fosfatidilcolinas/química , Porfirinas/química , Radiossensibilizantes/química , SuínosRESUMO
BACKGROUND This study was carried out to evaluate the effects of a long-term high-fat diet on lipids and lipoproteins composition in thoracic duct lymph in pigs. MATERIAL AND METHODS We examined lymph taken from the thoracic duct from 24 female white sharp-ear pigs, divided into 3 experimental groups fed different diets for 12 months: (a) the control group, fed the standard balanced diet; (b) the HFD group, fed an unbalanced, high-fat diet, and (c) the reversal diet group (RD), fed an unbalanced, high-fat diet for 9 months and then a standard balanced diet for 3 months. RESULTS Lymph analysis after 12 months of fixed diets revealed significantly higher concentration of proteins in the HFD group in comparison to the control and RD groups. Examination of lymph lipoproteins fractions showed that the high-fat diet in the HFD group in comparison to control group caused an increase in cholesterol, phospholipids, and proteins content within HDL and chylomicrons. There were also more proteins within HDL in the HFD group in comparison to the RD group and more triglycerides within chylomicrons in the HFD group in comparison to the control group. CONCLUSIONS A long-term high-fat diet resulted in changed structure of HDL and chylomicrons in the thoracic duct lymph. Alterations in HDL composition suggest that a high-fat diet enhances reverses cholesterol transport. Changes in chylomicrons structure show the adaptation to more intense transport of dietary fat from the intestine to the liver under the influence of a high-fat diet. Reversal to a standard balanced diet had the opposite effects.
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Dieta Hiperlipídica/efeitos adversos , Linfa/metabolismo , Ducto Torácico/metabolismo , Animais , Colesterol/metabolismo , Gorduras na Dieta/metabolismo , Feminino , Metabolismo dos Lipídeos/fisiologia , Lipídeos/análise , Lipídeos/fisiologia , Lipoproteínas/análise , Lipoproteínas/metabolismo , Lipoproteínas HDL/metabolismo , Lipoproteínas LDL/metabolismo , Fígado/metabolismo , Suínos/metabolismo , Ducto Torácico/efeitos dos fármacos , Triglicerídeos/análiseRESUMO
The early asymptomatic stage of glomerular injury is a diagnostic challenge in the course of renal and extra-renal disease, e.g., heart insufficiency. It was found that podocin, a podocyte-specific protein present in the urine, may serve as a biomarker in the diagnosis of glomerular disease in humans and animals including glomerulonephritis, glomerulosclerosis, amyloidosis, or nephropathy. Therefore, there is a need of development of the sensitive and straightforward method of urinary podocin identification. In this work, we report our extended research under the glomerular injury investigation in dogs by application of clinical examination and LC-MS-MRM method in the identification of canine podocin in urine samples. The LC-MS-MRM method is based on the identification of podocin tryptic peptide with the 218H-AAEILAATPAAVQLR-OH232 sequence. The model peptide was characterized by the highest ionization efficiency of all the proposed model podocin tryptic peptides in a canine urine sediment according to the LC-MS/MS analysis. The obtained results revealed the presence of the model peptide in 40.9% of dogs with MMVD (active glomerular injury secondary to heart disease = cardiorenal syndrome-CRS) and 33.3% dogs with chronic kidney disease. The potential applicability of the developed methodology in the analysis of podocin in canine urine sediments was confirmed.
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Síndrome Cardiorrenal/veterinária , Doenças do Cão/diagnóstico , Peptídeos e Proteínas de Sinalização Intracelular/química , Proteínas de Membrana/química , Peptídeos/urina , Insuficiência Renal Crônica/veterinária , Animais , Biomarcadores/urina , Síndrome Cardiorrenal/diagnóstico , Síndrome Cardiorrenal/urina , Cromatografia Líquida , Doenças do Cão/urina , Cães , Feminino , Peptídeos e Proteínas de Sinalização Intracelular/urina , Masculino , Proteínas de Membrana/urina , Podócitos/citologia , Podócitos/metabolismo , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/urina , Sensibilidade e Especificidade , Espectrometria de Massas em TandemRESUMO
This is an animal model study to investigate changes in hemostasis during endotoxemic shock and to determine whether the combination of inhaled nitric oxide (iNO) + intravenous hydrocortisone had an effect on clot formation and fibrinolysis. iNO selectively decreases pulmonary artery pressure, without affecting cardiac index or systemic vascular resistance; however, the results of studies on the possible consequences of iNO administration on coagulation are inconsistent and require further research. Thirty-four piglets were included. Administering endotoxin caused severe hypodynamic shock. Half of the animals received iNO (30 ppm) + hydrocortisone, starting 3 h after endotoxin infusion and continuing to the end of the study. All animals developed coagulation disorders, manifested by a tendency to hypocoagulation; at the same time, fibrinolysis was impaired. Coagulation and fibrinolysis disorders persisted after endotoxin infusion was discontinued, with worse severity in the animals that died before the study was terminated. Administering iNO + hydrocortisone did not cause further changes in coagulation and fibrinolysis parameters, either during or after the endotoxin challenge, suggesting that potential therapeutic interventions with iNO to lower pulmonary arterial pressure will not affect hemostasis.
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Coagulação Sanguínea , Modelos Animais de Doenças , Fibrinólise , Hidrocortisona , Óxido Nítrico , Choque Séptico , Tromboelastografia , Animais , Hidrocortisona/administração & dosagem , Hidrocortisona/uso terapêutico , Hidrocortisona/farmacologia , Óxido Nítrico/metabolismo , Fibrinólise/efeitos dos fármacos , Suínos , Coagulação Sanguínea/efeitos dos fármacos , Choque Séptico/tratamento farmacológico , Administração por Inalação , Endotoxinas/administração & dosagem , Humanos , Transtornos da Coagulação Sanguínea/tratamento farmacológicoRESUMO
Stenting in veterinary medicine has been a rapidly growing method of interventional surgery for several years. This procedure is usually performed in the respiratory and urinary tracts, but there are cases of stenting of blood vessels or gastrointestinal structures. It is based on maintaining the permeability of a given tubular structure, thus allowing the passage of gas or liquid. This procedure is often performed as a first-line treatment in situations where pharmacological agents do not work and as an alternative method, often cheaper than the classically performed ones. There are also cases where stenting is used as a palliative treatment, e.g., to enable defecation in colonic obstruction due to tumour infiltration of the colon wall. Stenting is often a life-saving or comfort-improving procedure for animals, but one should also be aware of possible postoperative complications and be prepared for any adversity. For this reason, this review provides an insight into the current knowledge in veterinary medicine about stenting and the consequences associated with this procedure.
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Microbial colonization in veterinary stents poses a significant and concerning issue in veterinary medicine. Over time, these pathogens, particularly bacteria, can colonize the stent surfaces, leading to various complications. Two weeks following the stent insertion procedure, the colonization becomes observable, with the aggressiveness of bacterial growth directly correlating with the duration of stent placement. Such microbial colonization can result in infections and inflammations, compromising the stent's efficacy and, subsequently, the animal patient's overall well-being. Managing and mitigating the impact of these pathogens on veterinary stents is a crucial challenge that veterinarians and researchers are actively addressing to ensure the successful treatment and recovery of their animal patients. In addition, irritation of the tissue in the form of an inserted stent can lead to overgrowth of granulation tissue, leading to the closure of the stent lumen, as is most often the case in the trachea. Such serious complications after stent placement require improvements in the procedures used to date. In this review, antibacterial or antibiofilm strategies for several stents used in veterinary medicine have been discussed based on the current literature and the perspectives have been drawn. Various coating strategies such as coating with hydrogel, antibiotic, or other antimicrobial agents have been reviewed.
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Hospital mortality in sepsis varies between 30-45%. It has been shown that administration of inhaled nitric oxide (iNO) and intravenous corticosteroid in a porcine endotoxemia model attenuated the systemic inflammatory response. We explored the anti-inflammatory effect of a double-treatment strategy (iNO + low-dose steroid) on the lungs in a long-term porcine endotoxic shock model. As metalloproteinases (MMPs) are involved in the initiation of multiple organ dysfunction in septic shock, we evaluated the influence of this combination therapy on MMP2 and MMP9 activity and proIL-1ß maturation. A shock-like condition was established in 23 animals by continuous infusion of E. coli lipopolysaccharide (LPS) for 10 h. Then the animals were observed for 10 h. Twelve pigs received iNO and hydrocortisone (iNO treatment started 3 h after the initial LPS infusion and continued until the end of the experiment). Eleven pigs were controls. Pigs treated with iNO and hydrocortisone displayed less inflammatory infiltrates in the lungs than the controls and a lower level of IL-1ß. The proMMP2 was significantly decreased in the iNO and hydrocortisone group. The amount of an active MMP9 (~ 60 kDa) was decreased in the iNO and hydrocortisone group. Total gelatinolytic activity was lower in the iNO and hydrocortisone group. Reduced MMP activity was accompanied by a 2.5-fold decrease of the active IL-1ß form (17 kDa) in the pulmonary tissue of iNO combined with hydrocortisone exposed pigs. We demonstrated that in a porcine endotoxemia model the NO inhalation combined with intravenous hydrocortisone led to the attenuation of the inflammatory cascade induced by bacterial LPS. The decrease in pulmonary MMPs activities was accompanied by reduced proIL-1ß processing.
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Endotoxemia , Sepse , Choque Séptico , Animais , Suínos , Hidrocortisona , Óxido Nítrico/farmacologia , Lipopolissacarídeos/farmacologia , Metaloproteinase 9 da Matriz/uso terapêutico , Endotoxemia/tratamento farmacológico , Endotoxemia/induzido quimicamente , Escherichia coli , Pulmão , Sepse/tratamento farmacológico , Choque Séptico/tratamento farmacológico , Administração por InalaçãoRESUMO
The decline in cardiac contractility due to damage or loss of cardiomyocytes is intensified by changes in the extracellular matrix leading to heart remodeling. An excessive matrix response in the ischemic cardiomyopathy may contribute to the elevated fibrotic compartment and diastolic dysfunction. Fibroproliferation is a defense response aimed at quickly closing the damaged area and maintaining tissue integrity. Balance in this process is of paramount importance, as the reduced post-infarction response causes scar thinning and more pronounced left ventricular remodeling, while excessive fibrosis leads to impairment of heart function. Under normal conditions, migration of progenitor cells to the lesion site occurs. These cells have the potential to differentiate into myocytes in vitro, but the changed micro-environment in the heart after infarction does not allow such differentiation. Stem cell transplantation affects the extracellular matrix remodeling and thus may facilitate the improvement of left ventricular function. Studies show that mesenchymal stem cell therapy after infarct reduces fibrosis. However, the authors did not specify whether they meant the reduction of scarring as a result of regeneration or changes in the matrix. Research is also necessary to rule out long-term negative effects of post-acute infarct stem cell therapy.
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INTRODUCTION: Myxomatous mitral valve disease (MMVD) in dogs inevitably causes renal dysfunction. These interactions are known as the cardiorenal syndrome (CRS). The main aims of the study were to evaluate whether renal resistive index (RRI) may be useful as a non-invasive marker in subclinical stage of kidney injury in dogs with MMVD and to compare RRI with SDMA and Cyst C. METHODS: Forty-four dogs were divided into two groups: control-15 healthy dogs and the heart group-29 dogs with MMVD (ACVIM class Cc). Study protocol included: anamnesis, clinical examination, electrocardiography, echocardiography, chest radiography, abdominal ultrasonography with measurements of the renal resistive index (RRI), urine, and blood analysis. RESULTS: The RRI in the heart group was significantly higher 0.725 ± 0.035 versus control group 0.665 ± 0.028 (p < 0.00085). The RRI cut-off point in dogs with stable chronic heart failure (CHF) under 8 years is 0.775, in older 0.64. RRI was similar in MMVD dogs treated with ACE-I + furosemide and dogs treated ACE-I + torasemide + pimobendan + spironolactone. There was no correlation between RRI and SDMA or Cyst C. CONCLUSION: RRI is more sensitive than creatinine, SDMA and Cyst C to reveal kidney injury in MMVD dogs class Cc younger than 8 years.
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Biomarcadores/metabolismo , Síndrome Cardiorrenal/diagnóstico , Síndrome Cardiorrenal/veterinária , Doenças das Valvas Cardíacas/diagnóstico , Doenças das Valvas Cardíacas/veterinária , Rim/patologia , Valva Mitral/patologia , Animais , Síndrome Cardiorrenal/sangue , Síndrome Cardiorrenal/diagnóstico por imagem , Cães , Feminino , Coração/diagnóstico por imagem , Doenças das Valvas Cardíacas/sangue , Doenças das Valvas Cardíacas/diagnóstico por imagem , Rim/diagnóstico por imagem , Modelos Logísticos , Masculino , Valva Mitral/diagnóstico por imagem , UltrassonografiaRESUMO
Animal nutrition plays an important role in the therapy of many diseases, including heart failure. The aim was to assess whether 6 months of feeding an AEP + ADH enriched diet (from fish meat) in dogs suffering from heart failure due to mitral degeneration impacts the dogs' metabolic profile and clinical status. Twenty small breed dogs were included: 50% were in stage B2 of MMVD and 50%, in stage C according to ACVIM. Dogs were randomly divided into two groups. One group receiving a standard diet, the second one a diet enriched with EPA + DHA (from fish meat). All dogs continued to receive appropriate therapy throughout the study. Control examinations were performed at the start of the study, after 3 and 6 months of appropriate feeding. Examinations included ECG, ECHO, blood hemathology and biochemistry, morphometric measurements, body fat index and subcutaneous fat tissue thickness. Serum samples were analyzed with a high-performance liquid chromatography system. Data were analyzed using the Progenesis QI (PQI, Non-linear Dynamics). The results showed no differences in clinical, cardiological, haematological and biochemical parameters between the two study groups. An effect on the metabolomic profile following a continued diet enriched in DHA + EPA (from fish meat) was more pronounced with time. After 6 months of feeding the diete enriched with DHA + EPA (from fish meat), there was a favorable reduction in glycerophosphocholine and xanthine levels, but an adverse increase in lactate and furvan and a decrease in alanine was not stopped.
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The diet is related to the diversity of bacteria in the oral cavity, and the less diverse microbiota of the oral cavity may favor the growth of pathogenic bacteria of all bacterial complexes. Literature data indicate that disturbances in the balance of the bacterial flora of the oral cavity seem to contribute to both oral diseases, including periodontitis, and systemic diseases. If left untreated, periodontitis can damage the gums and alveolar bones. Improper modern eating habits have an impact on the oral microbiome and the gut microbiome, which increase the risk of several chronic diseases, including inflammatory bowel disease, obesity, type 2 diabetes, cardiovascular disease and cancer. The subject of our consideration is the influence of the traditional diet on the formation of oxidative stress and inflammation caused by bacterial biofilm in the oral cavity. Through dental, biomedical and laboratory studies, we wanted to investigate the effect of individual nutrients contained in specific diets on the induction of oxidative stress inducing inflammation of the soft tissues in the oral cavity in the presence of residual supra- and subgingival biofilm. In our research we used different types of diets marked as W, T, B, F and noninvasively collected biological material in the form of bacterial inoculum from volunteers. The analyzed material was grown on complete and selective media against specific strains of all bacterial complexes. Additionally, the zones of growth inhibition were analyzed based on the disc diffusion method. The research was supplemented with dental and periodontological indicators. The research was supplemented by the application of molecular biology methods related to bacterial DNA isolation, PCR reactions and sequencing. Such selected methods constitute an ideal screening test for the analysis of oral bacterial microbiota. The obtained results suggest that certain types of diet can be an effective prophylaxis in the treatment of civilization diseases such as inflammation of the oral cavity along with periodontal tissues and gingival pockets.
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The article is a concise compendium of knowledge on the etiology of pathogenic microorganisms of all complexes causing oral diseases. The influence of particular components of the diet and the role of oxidative stress in periodontal diseases were described. The study investigated the bacteriostatic effect of the diet of adults in in vivo and in vitro tests on the formation of bacterial biofilms living in the subgingival plaque, causing diseases called periodontitis. If left untreated, periodontitis can damage the gums and alveolar bones. Anaerobic bacteria, called periopathogens or periodontopathogens, play a key role in the etiopathogenesis of periodontitis. The most important periopathogens of the oral microbiota are bacteria of all complexes, including the red complex. The obtained results suggest the possibility of using a specific diet in the prevention and treatment of periodontal diseases-already treated as a disease of civilization. The quoted article is an innovative compilation of knowledge on this subject and it can be a valuable source of knowledge for professional hygienists, dentists, peridontologists, dentistry students and anyone who cares about proper oral hygiene. The obtained results suggest the possibility of using this type of diet in the prophylaxis of the oral cavity in order to avoid periodontitis.
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Long-term high fat-carbohydrates diet (HF-CD) contributes to the formation of irreversible changes in the organism that lead to the emergence of civilization diseases. In this study, the impact of three-month high-fat diet on the physical properties of erythrocytes (RBCs) was studied. Furthermore, the biological activity of Cistus incanus L. extracts, plant known with high pro-health potential, in relation to normal and HF-CD RBCs, was determined. Obtained results have shown that, applied HF-CD modified shape, membrane potential and osmotic resistance of erythrocytes causing changes in membrane lipid composition and the distribution of lipids. The impact of HF-CD on physical properties of RBCs along with atherosclerotic lesions of the artery was visible, despite the lack of statistically significant changes in blood morphology and plasma lipid profile. This suggests that erythrocytes may be good markers of obesity-related diseases. The studies of biological activity of Cistus incanus L. extracts have demonstrated that they may ameliorate the effect of HF-CD on erythrocytes through the membrane-modifying and antioxidant activity.
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The literature suggests that strenuous exercise and exposure to high temperatures may cause physiologic proteinuria, but to our knowledge there have been no studies that have assessed the effect of high temperatures on the occurrence of post-exercise albuminuria in dogs. The goal of the study was to assess the impact of high temperatures on the occurrence of albuminuria. Thirteen healthy adult dogs-eight female (62%) and five male (38%) had to run 5 km at a temperature of 25 °C in grasslands which took about 30-40 min. Dogs underwent clinical examinations: echocardiography, abdominal ultrasound, blood hematology and biochemistry and urinalysis, including the ratio of albumin to creatinine (UAC). Baseline UAC was on the borderline of statistical significance for female dogs, but not for male dogs, before and after exercise. UAC was 0.31 ± 0.56 mg/mmol for female dogs and 0.36 ± 0.60 mg/mmol in male dogs before exercise. Immediately after exercise, UAC was 0.51 ± 0.58 mg/mmol in female dogs and 0.31 ± 0.40 mg/mmol in male dogs. Thus, a period of about 30-40 min of intensive exercise at high temperatures (25 °C) did not lead to increased albuminuria. This suggests that there is no need to limit the movement activity before urine tests in dogs, even at high temperatures, before urinalysis.
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Pressurized intrathoracic aerosol chemotherapy (PITAC) has been introduced to the clinical setting as a novel treatment option for pleural metastasis (PM). For decades the therapeutic application of aerosols was limited to intrabronchial delivery. However, present studies suggest performing PITAC on patients with PM and malignant pleural effusion. Using an established ex vivo swine model, the present study aimed to introduce a facilitated intrathoracic chemoaerosol application via spray-catheter. Using an ex-vivo model of 3 postmortem swine, the feasibility of intrathoracic aerosol chemotherapy (ITC) with doxorubicin using a spray-catheter was evaluated in a normal pressure environment. Following thoracotomy, the spray-catheter was inserted via trocar. Tissue samples were retrieved and further analyzed by fluorescence microscopy to detect doxorubicin contact. Our data demonstrated that the application of ITC was technically feasible and did not exhibit any significant obstacles. By making a minimally invasive thoracotomy incision it was possible to create an adequate pneumothorax without the need of a double-lumen tube or intubation. ITC did not require the creation of a pressurized environment. Tissue samples revealed doxorubicin contact within the pleura. In conclusion, ITC is a fast and feasible procedure that could possibly be administered via bedside application, therefore eliminating the need of an operating room and surgical staff. However, further studies are required to evaluate the safety of patients and physicians regarding this novel applicational modality. Nevertheless, the present study demonstrated that ITC may potentially be applied at bedside, an option that is particularly important for patients who do not qualify for PITAC procedures.
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INTRODUCTION: Pacemaker implantation is the only effective symptomatic treatment for life-threatening bradyarrhythmias. Major complications observed after implantation of cardiac pacemakers include lead dislocation, loss of pulse generator function, and inadequate stimulation. The aim of this retrospective single-centre study was to analyse the indications for pacemaker implantation and the incidence and types of complications associated with this procedure in dogs treated for symptomatic bradyarrhythmia. MATERIAL AND METHODS: The retrospective analysis included 31 dogs with symptomatic bradyarrhythmia, implanted with permanent cardiac pacemakers in 1992-2017. The list of analysed variables included patient age, breed, sex, indication for pacemaker implantation, comorbidities, and the incidence of procedure-related complications along with the type thereof. RESULTS: The most common indication for pacemaker implantation was 3rd degree AVB, followed by SSS, advanced 2nd degree AVB, and PAS. Pacemaker implantation was associated with a 35% overall complication rate and 6.45% periprocedural mortality. There were no significant differences in terms of procedure-related complications with regard to age, sex, breed, indications for pacemaker implantation, or comorbidities. CONCLUSIONS: Cardiac pacing is the only effective treatment of symptomatic bradycardia, but as an invasive procedure, may pose a risk of various complications, including death.