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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypothermic pulsatile perfusion did not adversely affect long-term renal allotransplant function and did not result in an increased rate of rejection. Thus, we can conclude that perfusion had little effect on the immunogenicity of renal allografts. The incidence of acute tubular necrosis was directly related to the length of warm ischaemia and perfusion time. However, long-term renal function was not influenced by acute tubular necrosis. Perfusion is a safe and reliable way of preserving cadaver donor kidneys until transplantation.
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PMID:Effect of organ preservation in cadaver kidney transplantation. 77 42

Experimental examinations were performed in 22 dogs to find out the mechanism which leads to a permanent or a reversible damage of the renal parenchyma after normo- and hypothermic ischemia. For this reason the perfusion and the distribution were examined with 133Xe, the vascular changes by angiography, and the parenchymal function with 131I-Hippuran. After normothermic ischemia a short-term reactive hyperemia appeared, which however could not compensate the damage of the renal tubular cells and the resulting excretory insufficiency. After hypothermic ischemia the perfusion was reduced, probably as a consequence of a vasconstriction by cold, however, the function of the tubular cells remained intact, because of the protective mechanism of the hypothermia. The importance of these findings for the development of the so-called "shock-kidney" (acute tubular necrosis) and for the conservative renal surgery in hypothermia is discussed and the application of measures beneficial to perfusion, are suggested.
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PMID:[Changes in perfusion and blood flow distribution following normo- and hypothermic ischemia of the kidneys]. 98 Jul 93

In this paper we describe the influence of ageing on responses to intravenously-injected endotoxin in two rat strains. Old age had no apparent effect on the absorption of 51Cr-labelled endotoxin from either jejunum or colon. Notwithstanding, aged animals appeared much more sensitive than their young counterparts to the lethal effects of intravenously injected endotoxin. Old animals exhibited virtually 100% mortality over the dose range 1-4 mg/100 g body weight while only sporadic deaths were seen in young animals. One consistent feature of dying animals was a profound and progressive hypothermia. At post mortem examination, the major findings were in the liver (leukocyte infiltrates and hepatocellular necrosis) and kidneys (acute tubular necrosis). Ageing was associated with slower removal of endotoxin from the circulation but not to an extent that could reasonably account for the enhanced sensitivity to endotoxin toxicity.
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PMID:Changes in endotoxin sensitivity in ageing. Absorption, elimination and mortality. 205 87

Calcium channel blockade has been shown to prevent warm renal ischemic damage. The ability of verapamil to decrease the severity of acute tubular necrosis (ATN) after 24-hr cold storage and autotransplantation was studied in a randomized paired study of 12 dogs. Experimental animals pretreated with intraarterial verapamil and flushing of the harvested kidney with cold intracellular solution containing verapamil demonstrated significantly (P less than .05) greater renal function preservation over their matched controls. A subsequent nonpaired study of 6 dogs treated only with flushing of the harvested kidney with perfusate containing verapamil demonstrated no significant preservation advantage over controls. We conclude that verapamil, administered prior to the ischemic event, can enhance the protective effect of hypothermia and decrease the severity of ATN in ischemically injured kidneys.
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PMID:The effect of verapamil in reducing the severity of acute tubular necrosis in canine renal autotransplants. 330 60

A total of 39 Holstein cattle were grazed in tracts of wild grassland on account of shortage in pasture grass. Twenty-nine cattle were affected and 26 of them died during a 21-day period. The main signs were depression, anorexia, ascites, and oliguria. There was elevated serum urea nitrogen and sugar and protein in the urine. Pathological examination revealed turbid swelling of the kidney, an increase in the amount of fluid in the body cavity, edema in the perirenal adipose tissue and hemorrhage in various visceral organs and tissues. Histologically, acute tubular necrosis in the kidney, hypoplasia of the erythroblast series in the bone marrow, atrophy and degeneration of the lymphatic tissue and focal necrosis of the liver were observed in many of the cattle. Among cows experimentally fed Narthecium asiaticum Maxim., Polygonum sachalinense Fr. Schum., and Vitis coignetiae Pulliat which were presumed to have been ingested in large amounts by grazing cattle in the field, the cows fed N. asiaticum revealed the clinical, biochemical and pathological changes similar to those noticed in naturally affected cattle. Cows fed P. sachalinense and V. coignetiae showed no distinct systemic symptoms except transient anorexia and hypothermia.
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PMID:Narthecium asiaticum Maxim. Poisoning of grazing cattle: observations on spontaneous and experimental cases. 398 97

The light and electron microscopic morphology of 57 cadaver renal allografts was assessed at the time of procurement and again after revascularization. Twenty-two kidneys (39%) did not function immediately after transplantation and 19 of these (86%) contained morphologic evidence of acute tubular necrosis (ATN) in the procurement biopsy. The morphology of the post-transplant biopsy was abnormal in all 22 kidneys with delayed function. There was a wide spectrum of morphologic change between the time of procurement and revascularization in all kidneys with normal function. These changes were mild in nature, were usually confined to proximal tubules, and were of unknown clinical significance. The morphology of kidneys that were damaged by the time of procurement was surprisingly different after storage with simple hypothermia (ice) than after storage with hypothermic pulsatile perfusion. The changes attributed to ice storage included endothelial swelling and vacuolation with obliteration and collapse of capillary lumens, fracture and splitting of peritubular basement membrane, and hyalinization of the renal interstitium. It was unknown whether these morphologic abnormalities were associated with delayed recovery of function of the injured kidneys.
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PMID:Renal allograft acute tubular necrosis. II. A light and electron microscopic study of biopsies taken at procurement and after revascularization. 634 15

The systemic symptoms, tissue lesions and release of cytokines were analysed in four isogenic mouse strains with distinct haplotypes injected with various doses of Loxosceles intermedia spider venom. The estimated LD50 were 24.5 microg for C57Bl/6, 17.6 microg for BALB/c, 6.3 microg for C3H/HeJ and 4.6 microg for A/Sn mice. Prostration, acute cachexia, hypothermia, neurological disorders and hemoglobinuria were the signals preceding death. Accumulation of eosinophilic material inside the proximal and distal renal tubules and acute tubular necrosis were the most common histopathological findings. Death was prevented by previous treatment of venom with specific antivenom serum. The protein F35 purified from the whole venom retained the ability to induce the symptoms of the whole venom. The cytokines tumor necrosis factor (TNF), interleukins IL-6 and IL-10 and the radical nitric oxide were detected in serum at different levels after venom injection. These findings indicate that the state of shock produced in mice by whole endotoxin-free L. intermedia venom or by its purified fraction, protein F35, mimics the endotoxemic shock, that susceptibility to the systemic effects of the venom varies among mice of different haplotypes and that the pattern of in vivo cytokine release resembles that of endotoxemic shock.
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PMID:Endotoxemic-like shock induced by Loxosceles spider venoms: pathological changes and putative cytokine mediators. 962 May 87

Although renal failure may occur following rewarming from deep accidental hypothermia, this subject has received little attention in experimental hypothermia and clinical case reports. In order to explore the integrity of hypothermic and posthypothermic renal morphology we used an experimental animal model of accidental hypothermia where the heart supports the circulation throughout cooling and rewarming without accompanying cardioplegia or ischemia. Ultrastructural changes in renal tubular cells from three groups of pentobarbital anesthetized Wistar rats: 1) controls (n=6) maintained at 37 degrees C for 4 h, 2) hypothermic rats (n=6) core-cooled and maintained at 15-13 degrees C for 4 h, and 3) rewarmed rats (n=10), were studied as a sensitive indicator of renal damage. Electron micrographs (EM) from hypothermic kidneys showed rounded up mitochondria with loss of contrast. These changes were observed in several though not all of the biopsies, but they were found in all kidneys. Areas exhibiting focal tubular necrosis were seen on most EM from three of these kidneys. EM from rewarmed kidneys showed alterations of mitochondrial ultrastructure with similarities to those observed after hypothermia, but in general the changes were more prominent. Extracellular edema, intracellular edema, swelling of mitochondria, margination of chromatin, necrosis of single tubular cells, and disrupting necrotic debris into tubular lumen could be found in micrographs from 7 of the 10 kidneys examined. Rewarming from experimental hypothermia, without episodes of ischemia or hypoxia, thus induces ultrastructural changes in renal tubular cells similar to changes observed in acute tubular necrosis, associated with renal failure.
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PMID:Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming. 1567 10

This paper describes clinical, laboratory and pathological findings of sheep, which is intoxicated with castor bean. The source of intoxication was a miscellaneous garden waste. Forty-five animals showed clinical toxicosis and 17 died. The clinical signs included weakness, salivation, profuse watery diarrhoea, dehydration, mydriasis, teeth grinding, hypothermia and recumbency. The most significant haematological and biochemical findings were a high haematocrit, high concentration of serum BUN, creatinine and phosphorus and high activity of serum CK and AST. Pathology revealed severe gastroenteritis, cardiac haemorrhage and necrosis, hepatic necrosis and acute tubular necrosis in kidneys. Treatment included symptomatic and supportive care with fluid therapy and cathartic administration.
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PMID:Castor bean (Ricinus communis) toxicosis in a sheep flock. 1715 90

Patient maintenance after successful cardiopulmonary resuscitation starts with decreasing the neurological damage despite serious difficulties such as hypoxic ischemic infarcts and reperfusion infarcts. Therapeutic hypothermia is the most rejoicing method in use to prevent neurological damage. Here, we discuss about a 35-year-old woman resuscitated for 20 minutes in hospital who was followed because of postpartum cardiomyopathy. Sudden onset of ventricular fibrillation subsequent to ventricular tachycardia was the underlying cause of cardiac arrest. To prevent neurological damage, therapeutic hypothermia was used, and she was cooled for 24 hours. After therapeutic hypothermia, her Glasgow coma score was 15, fortunately no sequela appeared. Although we were successful to prevent neurological damage, rhabdomyolysis arose secondary to therapeutic hypothermia. As a result, the intubation process was prolonged, and acute tubular necrosis due to myoglobinuria was occurred. Despite all complications patient faced, she was discharged on her 31th day; without sequela and with no need for hemodialysis; under medical therapy.
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PMID:Rhabdomyolysis Secondary to Therapeutic Hypothermia After Cardiopulmonary Resuscitation: A Rare Complication. 2629 13


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