RESUMEN
BACKGROUND: The University of Wisconsin (UW) solution is the gold standard for preserving the liver, kidneys, and pancreas. For renal preservation, the addition of the flavonoid, quercetin (QE), to the preservation solution reduces damage to renal tubular cells, and the addition of sucrose (Suc) is also beneficial for preservation. The aim of this study was to investigate the protective effects of QE and Suc on porcine livers in terms of warm and cold injury and to evaluate whether their use improves ischemia-reperfusion (I/R) injury after simple cold storage (CS). METHODS: We tested porcine livers procured after 30 minutes of warm ischemia followed by preservation for 6 hours under the following 2 conditions: group 1, preserved with the CS/UW solution (n = 4); group 2, preserved with the CS/UW solution containing Que 33.1 µM and Suc 0.1 M (n = 6). All livers were evaluated using an ex vivo isolated liver reperfusion model with saline-diluted autologous blood. RESULTS: Aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase levels in group 2 were significantly lower at 30 minutes of reperfusion than in group 1. Furthermore, histologic evaluation by hematoxylin and eosin staining showed significantly fewer morphologic changes in group 2 than in group 1, as indicated by the total Suzuki score. Group 2 also had significantly better scores for sinusoidal congestion and hepatocyte cytoplasmic vacuolization. CONCLUSION: Adding Que and Suc to the UW solution can effectively prevent cold injury in livers donated after circulatory death.
Asunto(s)
Lesión por Frío , Soluciones Preservantes de Órganos , Daño por Reperfusión , Humanos , Porcinos , Animales , Preservación de Órganos , Quercetina/farmacología , Soluciones Preservantes de Órganos/farmacología , Hígado/patología , Daño por Reperfusión/etiología , Daño por Reperfusión/prevención & control , Daño por Reperfusión/patología , Glutatión/farmacología , Alopurinol/farmacología , Insulina/farmacología , Rafinosa/farmacología , Lesión por Frío/patologíaRESUMEN
Traumatic brain injury (TBI) is the most prevalent health problem affecting all age groups, and leads to many secondary problems in other organs especially kidneys, gastrointestinal tract, and heart function. In this review, the search terms were TBI, fluid percussion injury, cold injury, weight drop impact acceleration injury, lateral fluid percussion, cortical impact injury, and blast injury. Studies with Actaea racemosa, Artemisia annua, Aframomum melegueta, Carthamus tinctorius, Cinnamomum zeylanicum, Crocus sativus, Cnidium monnieri, Curcuma longa, Gastrodia elata, Malva sylvestris, Da Chuanxiong Formula, Erigeron breviscapus, Panax ginseng, Salvia tomentosa, Satureja khuzistanica, Nigella sativa, Drynaria fortune, Dracaena cochinchinensis, Polygonum cuspidatum, Rosmarinus officinalis, Rheum tanguticum, Centella asiatica, and Curcuma zedoaria show a significant decrease in neuronal injury by different mechanisms such as increasing superoxide dismutase and catalase activities, suppressing nuclear factor kappa B (NF-κB), interleukin 1 (IL-1), glial fibrillary acidic protein, and IL-6 expression. The aim of this study was to evaluate the neuroprotective effects of medicinal plants in central nervous system pathologies by reviewing the available literature.
Asunto(s)
Traumatismos por Explosión/prevención & control , Lesiones Traumáticas del Encéfalo/prevención & control , Lesión por Frío/prevención & control , Regulación de la Expresión Génica/efectos de los fármacos , Fármacos Neuroprotectores/farmacología , Plantas Medicinales/química , Animales , Traumatismos por Explosión/genética , Traumatismos por Explosión/metabolismo , Traumatismos por Explosión/patología , Lesiones Traumáticas del Encéfalo/genética , Lesiones Traumáticas del Encéfalo/metabolismo , Lesiones Traumáticas del Encéfalo/patología , Catalasa/genética , Catalasa/metabolismo , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/lesiones , Corteza Cerebral/metabolismo , Lesión por Frío/genética , Lesión por Frío/metabolismo , Lesión por Frío/patología , Modelos Animales de Enfermedad , Proteína Ácida Fibrilar de la Glía/genética , Proteína Ácida Fibrilar de la Glía/metabolismo , Humanos , Interleucina-1/genética , Interleucina-1/metabolismo , Interleucina-6/genética , Interleucina-6/metabolismo , Ratones , FN-kappa B/genética , FN-kappa B/metabolismo , Fármacos Neuroprotectores/aislamiento & purificación , Ratas , Superóxido Dismutasa/genética , Superóxido Dismutasa/metabolismoRESUMEN
Alendronate, a nitrogen-containing bisphosphonate, is well established as a treatment for osteoporosis through regulation of osteoclast activity. Previously, the pharmacological effects of bisphosphonates on cells outside the bone environment have been considered irrelevant because bisphosphonates target bone. Here we show that administration of alendronate impairs muscle regeneration in mice after bone fracture. A series of injections of alendronate alone or bone fracture alone did not affect muscle regeneration induced by cold injury. In contrast, alendronate treatment plus bone fracture severely impaired the regeneration of muscle that closely contacts the bone fracture site after cold injury. After cold injury, M-cadherin-positive myogenic cells disappeared in the damaged muscle areas of mice receiving the combination of alendronate treatment and bone fracture. The present results suggest that the muscle regeneration capacity is impaired by bone fracture in mice receiving alendronate treatment. The present research on the pharmacological effects of alendronate on muscle regeneration will aid in understanding of the in vivo action of alendronate on skeletal muscles.
Asunto(s)
Alendronato/farmacología , Conservadores de la Densidad Ósea/farmacología , Lesión por Frío/fisiopatología , Fracturas Óseas/terapia , Músculo Esquelético/fisiopatología , Regeneración/fisiología , Alendronato/efectos adversos , Animales , Conservadores de la Densidad Ósea/efectos adversos , Lesión por Frío/patología , Lesión por Frío/terapia , Modelos Animales de Enfermedad , Fracturas Óseas/patología , Fracturas Óseas/fisiopatología , Masculino , Ratones Endogámicos ICR , Músculo Esquelético/efectos de los fármacos , Músculo Esquelético/patología , Regeneración/efectos de los fármacosAsunto(s)
Lesión por Frío/patología , Dermatosis Facial/patología , Hielo/efectos adversos , Conducta Autodestructiva , Enfermedades Cutáneas Vesiculoampollosas/patología , Piel/patología , Cloruro de Sodio/efectos adversos , Biopsia , Niño , Lesión por Frío/etiología , Frío , Dermatosis Facial/etiología , Femenino , Humanos , Umbral del Dolor , Valor Predictivo de las Pruebas , Enfermedades Cutáneas Vesiculoampollosas/etiología , Sensación TérmicaRESUMEN
Localized thermal injuries in animals may be caused by exposure to fire and radiant heat, contact with hot items including hot liquids or steam, inhalation of hot air, and exposure to cold temperatures. In addition, animal fire victims may have intoxications caused by smoke gas. This article reviews the causes, pathogenetic aspects, morphological findings, additional investigations, differential diagnoses, and causes of death in various forms of thermal injuries. Since these cases do not occur frequently in diagnostic pathology, they represent a challenging task in general but also with respect to forensic or criminal aspects, such as whether a lesion represents an accidental or nonaccidental effect. Besides detailed information about the circumstances at the location, thermal injuries in animals require a thorough morphological evaluation, including additional investigations in conjunction with a profound knowledge about the possible lesion spectrum and suitable additional investigations.
Asunto(s)
Quemaduras/veterinaria , Lesión por Frío/veterinaria , Patologia Forense/métodos , Trastornos de Estrés por Calor/veterinaria , Hipotermia/veterinaria , Patología Veterinaria/métodos , Animales , Autopsia/veterinaria , Quemaduras/diagnóstico , Quemaduras/patología , Causas de Muerte , Lesión por Frío/diagnóstico , Lesión por Frío/patología , Trastornos de Estrés por Calor/diagnóstico , Trastornos de Estrés por Calor/patología , Hipotermia/diagnóstico , Hipotermia/patologíaRESUMEN
BACKGROUND: A longstanding goal in regenerative medicine is to reconstitute functional tissues or organs after injury or disease. Attention has focused on the identification and relative contribution of tissue specific stem cells to the regeneration process. Relatively little is known about how the physiological process is regulated by other tissue constituents. Numerous injury models are used to investigate tissue regeneration, however, these models are often poorly understood. Specifically, for skeletal muscle regeneration several models are reported in the literature, yet the relative impact on muscle physiology and the distinct cells types have not been extensively characterised. METHODS: We have used transgenic Tg:Pax7nGFP and Flk1GFP/+ mouse models to respectively count the number of muscle stem (satellite) cells (SC) and number/shape of vessels by confocal microscopy. We performed histological and immunostainings to assess the differences in the key regeneration steps. Infiltration of immune cells, chemokines and cytokines production was assessed in vivo by Luminex®. RESULTS: We compared the 4 most commonly used injury models i.e. freeze injury (FI), barium chloride (BaCl2), notexin (NTX) and cardiotoxin (CTX). The FI was the most damaging. In this model, up to 96% of the SCs are destroyed with their surrounding environment (basal lamina and vasculature) leaving a "dead zone" devoid of viable cells. The regeneration process itself is fulfilled in all 4 models with virtually no fibrosis 28 days post-injury, except in the FI model. Inflammatory cells return to basal levels in the CTX, BaCl2 but still significantly high 1-month post-injury in the FI and NTX models. Interestingly the number of SC returned to normal only in the FI, 1-month post-injury, with SCs that are still cycling up to 3-months after the induction of the injury in the other models. CONCLUSIONS: Our studies show that the nature of the injury model should be chosen carefully depending on the experimental design and desired outcome. Although in all models the muscle regenerates completely, the trajectories of the regenerative process vary considerably. Furthermore, we show that histological parameters are not wholly sufficient to declare that regeneration is complete as molecular alterations (e.g. cycling SCs, cytokines) could have a major persistent impact.
Asunto(s)
Modelos Animales , Músculo Esquelético/fisiología , Regeneración , Animales , Compuestos de Bario/toxicidad , Cloruros/toxicidad , Proteínas Cardiotóxicas de Elápidos/toxicidad , Lesión por Frío/patología , Lesión por Frío/fisiopatología , Citocinas/fisiología , Venenos Elapídicos/toxicidad , Fibrosis , Congelación/efectos adversos , Proteínas Fluorescentes Verdes/análisis , Macrófagos/fisiología , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Desarrollo de Músculos , Músculo Esquelético/efectos de los fármacos , Músculo Esquelético/lesiones , Músculo Esquelético/patología , Mioblastos/fisiología , Necrosis , Neovascularización Fisiológica , Regeneración/inmunología , Regeneración/fisiología , Células Satélite del Músculo Esquelético/fisiología , Células Madre/fisiología , Receptor 2 de Factores de Crecimiento Endotelial Vascular/análisisRESUMEN
Subtle blood-brain barrier (BBB) disruption is involved in numerous neurological conditions. This disruption is found diffusely in the brain and requires quantitative methods for assessment. We propose a statistical method to identify individual voxels where the BBB is disrupted using T1-weighted MRI. We used models of severe and focal vs. mild and generalized disruption of the BBB to show proof of principle with the cold injury model, hypoxia, and a model of inflammation using low- and high-dose lipopolysaccharide (LPS) treatment. Using voxel-based analysis, we found that mild hypoxia resulted in diffuse disruption of the BBB, whereas more severe hypoxia and high-dose LPS treatment resulted in prominent leakage, particularly in the periventricular area, suggestive of blood-cerebrospinal fluid (CSF) barrier disruption. Our data suggest that the periventricular area may be compromised first in conditions of inflammation and hypoxia. Voxel-based analysis could be used in future studies assessing subtle blood-CSF or BBB disruption.
Asunto(s)
Barrera Hematoencefálica/metabolismo , Encéfalo/metabolismo , Líquido Cefalorraquídeo/metabolismo , Lesión por Frío/metabolismo , Hipoxia/metabolismo , Inflamación/metabolismo , Animales , Barrera Hematoencefálica/diagnóstico por imagen , Barrera Hematoencefálica/efectos de los fármacos , Barrera Hematoencefálica/patología , Encéfalo/efectos de los fármacos , Encéfalo/patología , Líquido Cefalorraquídeo/diagnóstico por imagen , Líquido Cefalorraquídeo/efectos de los fármacos , Lesión por Frío/diagnóstico por imagen , Lesión por Frío/patología , Medios de Contraste , Modelos Animales de Enfermedad , Gadolinio , Hipoxia/diagnóstico por imagen , Hipoxia/patología , Inflamación/inducido químicamente , Inflamación/diagnóstico por imagen , Inflamación/patología , Lipopolisacáridos/farmacología , Imagen por Resonancia Magnética , Masculino , Ratas , Ratas WistarAsunto(s)
Lesión por Frío/patología , Frío/efectos adversos , Eritema/patología , Anciano , Femenino , Humanos , Estaciones del Año , MusloRESUMEN
In experiment on animals, in which the cold trauma was simulated, the systemic inflammatory reactions indiceslevel of Сreactive protein, аctive products of thiobarbituric acid the blood serum, erythrocyte sedimentation rate (ESR), leukocyte blood formula (LBF) while injection of placenta extract were studied. Creactive protein level lowering in 1.3 times on the 14th day of experiment, reduction of ESR in 1.6 times on the 7th and 14th day, LBF normalization on the 7th day, lowering of the аctive products of thiobarbituric acid level in 1.3 times on the 7, 9th and 14th day of observation were noted. On the 21st day all the indices came back to norm.