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

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.
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PMID:Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs. 236 Jun 37

A recent study from our laboratory revealed that cotreating mice with the alpha-adrenoreceptor antagonists phentolamine and idazoxan markedly diminished bromobenzene-induced hepatotoxicity. Subsequent studies also revealed that such cotreatment does not alter the pharmacokinetic disposition of bromobenzene in mice nor its bioactivation to reactive metabolites. In the present study, the possible role of hypothermia in the phentolamine antagonism of bromobenzene-induced hepatotoxicity was investigated. Bromobenzene alone caused a significant, dose-related hypothermia. The high dosage regimen (10 mg/kg per dose) of phentolamine or idazoxan that had been found to be hepatoprotective in earlier studies potentiated this hypothermia and more than doubled the net decrease in core body temperature experienced by the animals. Placing mice receiving bromobenzene in an environment with an ambient temperature of 10 degrees C likewise increased the hypothermia experienced by animals receiving bromobenzene. The magnitude of the net change in core body temperature elicited by exposure to cold was similar to but slightly less than the net change produced by cotreatment with either alpha-adrenoreceptor antagonist and the magnitude of the hepatoprotection this procedure provided against bromobenzene hepatotoxicity was equivalent to that observed with phentolamine cotreatment. In contrast, a lower dosage regimen of either adrenoreceptor antagonist (2.5 mg/kg per dose) resulted in no additional hypothermia yet still produced a near maximal antagonism of bromobenzene-induced hepatotoxicity. Further, increasing the ambient temperature to 30 degrees C completely reversed the phentolamine-induced (10 mg/kg per dose) increase in hypothermia, but did not affect phentolamine's antagonism of the bromobenzene-induced changes in hepatic glutathione levels, serum alanine aminotransferase activity, or 24-hr mortality. Therefore, we conclude that while the hepatoprotective intervention of phentolamine can be mimicked by an exposure to cold that results in hypothermia, it is clear that alpha-adrenergic antagonists diminish the hepatotoxicity induced by bromobenzene by a mechanism that is independent of hypothermia.
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PMID:Antagonism of bromobenzene-induced hepatotoxicity by the alpha-adrenoreceptor blocking agents phentolamine and idazoxan: role of hypothermia. 256 19

Studies have been made on the activity of aspartate and alanine aminotransferase in the brain of 1, 4, 12-14, 16, 22 days, 1, 1 1/2, 3 months and 2 years old rats under hypothermic conditions (20-19 degrees C). It was shown that hypothermia decreases both total and specific activities of the enzymes in the developing brain. Alanine aminotransferase activity in brain homogenates determined at 37 and 20-19 degrees C, exhibits more significant changes than of aspartate aminotransferase.
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PMID:[Aminotransferase activity in the brain of rats of various ages during hypothermia]. 401 66

In a prospective study, 93 patients were observed up to nine months after open-heart surgery using hypothermia, hemodilution and cold cardioplegia. In the first two weeks frequent determinations were made of serum aminotransferase, alkaline phosphatases (ALP), lactic dehydrogenase isoenzymes, gamma glutamyltransferase (GT), total and free bilirubin and bile acids. Plasma hemoglobin was measured at the end of the operation. After the first period, aminotransferases, alkaline phosphatases and bilirubin were determined monthly. On the first postoperative day almost all of the patients showed abnormal aspartate aminotransferase (ASAT) activity and ASAT/ALAT (alanine aminotransferase) greater than 1, and about 25% had hyperbilirubinemia. The findings suggested early postoperative leakage of enzymes not only from the myocardium, but also from the liver. After two weeks the patients presented another pattern of liver dysfunction, with abnormal ALAT in 50%, ASAT/ALAT less than 1, and abnormal ALP and GT in 28 and 45%, respectively. Eight patients were judged to have post-transfusion hepatitis of non-A, non-B type. Six of them had abnormal aminotransferases for more than six months.
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PMID:Hepatic dysfunction after open-heart surgery. 615 78

We employed a bile duct ligation (BDL) model of cholestatic liver injury to test the hypothesis that this form of preexisting hepatic dysfunction alters the kinetics of circulating TNF-alpha and IL-6 after Escherichia coli endotoxemia, thereby augmenting mortality and lung injury by a TNF-alpha:leukotriene (LT) axis of inflammation. Male rats were catheterized 13 d after BDL or sham surgery and studied while awake 18 to 24 h later. Cholestasis after BDL was confirmed by baseline serum bilirubin (BDL = 7.34 +/- 0.72 mg/dl, mean +/- SEM, n = 17 versus Sham = 0.25 +/- 0.07, n = 20; p < 0.005) and histopathology. Sham and BDL animals received E. coli lipopolysaccharide serotype O55:B5 (LPS, 5 mg/kg i.v.) or 0.9% NaCl (NS) ending at t = 0 and were monitored over 24 h for vital signs and hemodynamics. In parallel studies, lipoxygenase inhibition was performed using diethylcarbamazine or the 5-lipoxygenase activating-protein inhibitor MK-886. Blood was collected at baseline and at t = 1.5, 3.5, and 24 h for formed elements and for serum endotoxin, TNF-alpha, IL-6, bilirubin, and alanine aminotransferase (ALT). Organs were evaluated at 24 h for histopathology, including neutrophil (PMN) densities and wet/dry weight (W/D) ratios. Cholestasis reduced survival after otherwise nonlethal endotoxemia, with seven of 11 BDL + LPS rats dying within 24 h versus no deaths in BDL + NS (n = 6), Sham + LPS (n = 14), or Sham + NS (n = 6) animals (p < 0.01). Despite equivalent serum endotoxin between groups, circulating TNF-alpha was 8-fold higher in BDL + LPS than in Sham + LPS rats at 1.5 and 3.5 h (p < 0.001), whereas serum TNF-alpha did not differ between BDL + NS and Sham + NS rats. IL-6 likewise was increased differentially by 1.5 h in BDL + LPS animals (11.98 +/- 2.42 ng/ml) versus Sham + LPS rats (3.05 +/- 0.58 ng/ml, p < 0.05). Hypothermia, bradycardic hypotension, and leukopenia were most severe and prolonged in BDL + LPS rats, which also had significantly higher ALT values, W/D ratios, and organ PMN counts. LT inhibition failed to reduce BDL-related differences in serum cytokines or survival after endotoxemia. Thus, cholestasis augments inflammatory responses to gram-negative endotoxemia, sensitizing the host to enhanced fluid flux in multiple organs and to mortality by a LT-independent mechanism.
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PMID:Cholestatic liver injury increases circulating TNF-alpha and IL-6 and mortality after Escherichia coli endotoxemia. 960 37

The quality of cold-stored donor livers slowly declines beyond approximately 12 h, although these organs may still be used for clinical transplantation. The aim of the present study was to improve the energetic status and viability of long-term-preserved livers by short-term gaseous oxygen insufflation prior to implantation of the organ using a technique that has already been shown to promote aerobic energy metabolism during hypothermia. Livers from ten male Wistar rats were isolated, rinsed blood-free. Five livers (group 1) were stored for 48 h at 4 degrees C in UW preservation solution, and five livers (group 2) were isolated and stored in the same manner for 47 h, and were then, during the last 60 min of the preservation period, connected to a persufflation device and gaseous oxygen was introduced into the organ via the inferior caval vein, with the liver still immersed in cold UW solution. This technique of endischemic gaseous oxygenation resulted in a significant normalization of vascular resistance upon isolated reperfusion in vitro and a reduction in hepatic efflux of alanine aminotransferase as well as glutamate dehydrogenase, which led to improved recovery of the reperfused grafts of group 2 as evidenced by an elevated energy charge potential at the end of the reperfusion period. In conclusion, the technique described seemed effective in enhancing the preoperative viability of marginal donor grafts.
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PMID:Endischemic oxygen persufflation to improve viability of marginally preserved donor livers. 966 26

This study was designed to elucidate the efficacy of University of Wisconsin (UW) solution for preventing liver injury, when used as a hypothermic perfusate infused into the systemic circulation during extended hepatectomy with hepatic inflow occlusion. Adult mongrel dogs (9.5-17.5 kg, n = 14) were subjected to 75% hepatectomy under 60 min hepatic inflow occlusion. The animals were divided into two groups. The UW group (n = 7) underwent hypothermic perfusion using 4 degrees C UW solution (core temperature of the liver: 12.3 +/- 0.2 degrees C). The control group designated as the Ringer's lactate (LR) group (n = 7) underwent hypothermic perfusion using 4 degrees C LR solution. The perfusate was introduced into the systemic circulation via the hepatic vein. Blood from the hepatic vein was sampled, and alanine aminotransferase, purine nucleoside phosphorylase activities and the ammonia concentration were measured. The 7 day survival rate was higher in the UW group than in the LR group. The parameters of liver function were less significantly altered in the UW group than in the LR group. The plasma ammonia concentration was significantly (P < 0.05) lower 6 h after reperfusion in the UW group than in the LR group. A small volume of hypothermic perfusion of the liver using UW solution was safe if it returned to systemic circulation. Hypothermic perfusion of the liver using UW solution may be effective for preventing hepatic tissue injury during extended hepatectomy with hepatic vascular occlusion.
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PMID:Efficacy of hypothermic perfusion using University of Wisconsin solution in extended hepatectomy with hepatic inflow occlusion in a canine model. 973 70

Accidental hypothermia is a common companion of trauma/haemorrhage, and several clinical studies have identified reduced body temperature as an independent risk predisposing to increased morbidity and mortality. Accordingly, the majority of trauma care guidelines prescribe early and aggressive rewarming of hypothermic patients. Enzyme reactions are generally downregulated at temperatures below 37 degrees C, including most of those responsible for the inflammatory response. The rationale for adhering to these recommendations uncritically may therefore be questioned. In a rat model of mild hypothermia and haemorrhagic shock we wanted to compare the influence of rapid rewarming with persistently reduced temperature on the synthesis of early inflammatory mediators and organ function. Thirty-four male albino Sprague-Dawley rats were studied. Withdrawal of 2.5 ml blood/100 g body weight was performed over 10 min, with simultaneous reduction of body temperature to 32.5-33.5 degrees C. Seventy-five minutes after initiation of bleeding, two-thirds of the shed blood was retransfused. One group (n=17) was rewarmed to normothermia, the other (n=17) was kept hypothermic. The study was terminated after an observation period of 2 h. At the end of the study the rewarmed animals had a significantly lower mean arterial pressure, higher heart rate, higher synthesis of reactive oxygen species from peritoneal phagocytes, increased circulating levels of nitric oxide, and higher values of the organ markers aspartate aminotransferase and urea. The pro-inflammatory cytokines TNF-alpha and IL-6, the anti-inflammatory cytokine IL-10, the organ markers alanine aminotransferase, alpha-glutathione S-transferase and creatinine, as well as organ injury scores were equal in both groups. Three rewarmed rats died prematurely, versus one hypothermic animal. In conclusion, the results suggest that during the early stages after haemorrhagic shock, rapid rewarming from mild hypothermia may have unfavourable effects both on basic haemodynamic variables, and on the internal inflammatory environment of cells and tissues.
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PMID:Rapid rewarming after mild hypothermia accentuates the inflammatory response after acute volume controlled haemorrhage in spontaneously breathing rats. 1286 16

The aim of this study was to evaluate effect of a short-acting neuroleptic (acepromazine) on capture stress response in roe deer (Capreolus capreolus). Sixteen roe deer were captured by drive-nets in the winters of 1998, 1999, and 2001. Roe deer were divided into two groups: animals in the treatment group received an intramuscular injection of acepromazine (0.093 mg/kg +/- 0.003 SEM; n = 8) while animals in the control group (n = 8) did not receive tranquilizer. Heart rate and body temperature, as well as hematologic and biochemical indicators of stress, were used to evaluate effect of the neuroleptic over 3 hr. Heart rate decreased over time after capture in both groups (P < 0.05), but stabilized sooner in the treated roe deer (75 min after capture) than in the controls (105 min after capture). Body temperature decreased over 45 min and then stabilized in both groups (P < 0.05). Comparisons of blood parameters revealed significantly lower red blood cell count (RBC), lymphocyte count, hemoglobin concentration, packed cell volume (PCV), and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatine kinase (CK), and lactate dehydrogenase (LDH) activities in tranquilized animals compared with controls (at least P < 0.05). A reduction in PCV, lymphocyte count, and serum cortisol concentrations (at least P < 0.05) and an increase in serum creatinine levels (P < 0.05) were recorded over time in control animals, while a reduction in RBC and hemoglobin concentration (at least P < 0.05) and an increase in serum urea concentrations (P < 0.05) over time were observed in the treated group. Finally, a decrease in serum lactate and potassium levels and an increase in CK, AST, ALT, and LDH activities were recorded over time in both groups. Results obtained showed the suitability of using acepromazine in capture operations in order to reduce stress response and prevent its adverse effects in roe deer. The beneficial effect was not only due to the sedative effect of acepromazine, but also to peripheral vasodilatation.
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PMID:Effects of acepromazine on capture stress in roe deer (Capreolus capreolus). 1291 Jul 65


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