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

The phospholipid bilayer of the plasma membrane plays an important role in forming a functional barrier against leakage of ions and other cell constituents. We have examined the effect of an exogenously added phospholipase C (PLC) on phospholipid degradation in isolated rat myocardial cells subjected to hypothermia (5 degrees C) and hypothermia followed by rewarming to 37 degrees C. The activity of PLC was measured as glycerol output to the incubation medium since the combined action of PLC and endogenous lipases will result in glycerol production. Addition of PLC resulted in a significantly higher output of glycerol in rewarmed myocytes than in myocytes kept constantly at 5 degrees C and 37 degrees C. Rewarmed cells also showed the highest leakage of lactate dehydrogenase (LDH), but there was no additional effect of PLC on LDH leakage. Normal levels of cellular ATP were maintained in all myocyte groups. These results show that rewarming from hypothermia may cause structural derangements in the phospholipid bilayer of the sarcolemma which in turn could favor attack by endogenous phospholipases.
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PMID:Membrane phospholipid metabolism of rat myocardial cells during hypothermia and rewarming. 181 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

To test the hypothesis that hypothermia prevents myocardial Ca2+ loading during reoxygenation, we examined the effects of 2 h of hypoxia with and without hypothermia on the Ca2+ content of cultured chick embryo ventricular cells. When compared with hypoxic cells at 37 degrees C, hypoxia at 11 degrees C (hypothermia) augmented the 45Ca content of cardiocytes after 30 min of normothermic reoxygenation from 3.85 +/- 0.2 to 4.7 +/- 0.1 nmol/mg protein (P less than 0.001). The Na+ content of hypoxic myocytes was also increased at the end of 2 h of hypoxia from 648 +/- 59 to 1,026 +/- 68 nmol/mg protein in cells exposed to hypoxia at 11 degrees C (P less than 0.001). Hypothermia ameliorated hypoxia-induced depression of cellular ATP content and did not result in significant membrane injury as determined by lactate dehydrogenase release. These data indicate that hypothermia augments rather than decreases the Ca2+ content of hypoxic myocytes during reoxygenation after hypoxia. Ca2+ loading appears to be secondary to an increase in Na+ content, creating a favorable gradient for Ca2+ influx through Na(+)-Ca2+ exchange or an unfavorable gradient for Ca2+ extrusion.
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PMID:Hypothermia increases calcium content of hypoxic myocytes. 238 17

Hepatocytes from isolated rat livers were hypothermically incubated (5 degrees C) in an oxygenated environment with continuous shaking (to simulate organ perfusion preservation). The incubation solution was either a tissue culture medium (L-15), an organ preservation perfusate (UW gluconate), or a simple cold-storage solution used for organ preservation (UW lactobionate). Hepatocyte viability was assessed from the release of lactate dehydrogenase (LDH) into the incubation medium. Cell swelling (due to the uptake of water) was also measured. Within 24 hr, hepatocytes hypothermically stored in each of the three incubation solutions became swollen (30 to 40% water gain) and lost a significant amount of LDH (as much as 60%). The addition of polyethylene glycol (PEG; relative molecular mass 8000; 5 g%) to the solutions suppressed cell swelling and allowed the incubated hepatocytes to remain relatively well preserved (30% LDH release) for as long as 120 hr. Adding either dextran (relative molecular mass 10,000 to 78,000; 5 g%) or saccharides (100 mmol/liter) instead of PEG neither prevented cell swelling nor prevented the cells from dying. The results of this study suggest (i) there is a direct correlation (r = 0.873) between hypothermia-induced cell swelling and cell death (i.e., the suppression of cell swelling prevents cell death); (ii) the mechanism by which PEG prevents cell swelling (and thus maintains cell viability) is not related to the osmotic or oncotic properties of the molecule but instead is apparently related to some unknown interaction between PEG and the cell, an interaction that provides stability during hypothermic incubation; and (iii) hypothermia-induced cell swelling must be prevented if isolated hepatocytes are to be used as a model for studying the mechanism by which cell damage occurs during hypothermic organ preservation. By eliminating cell death due to cell swelling, the biochemical mechanisms of cell death can be studied.
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PMID:Hypothermic preservation of hepatocytes. I. Role of cell swelling. 248 Aug 65

We serially measured creatine kinase (CK), lactate dehydrogenase, aspartate aminotransferase (AST) and lactate from the lumbar cerebrospinal fluid in 14 patients with neurologic complications after open heart surgery with cardiopulmonary bypass (CPB). These analyses revealed a correlation between worsening neurologic deficit and the peak CK (r = .87, p less than .001), AST (r = .75, p less than .01), and lactate (r = .93, p less than .001) levels. Lactate increased before enzymes did. In 12 patients without complications, only lactate was significantly (p less than .005) elevated; however, within this group, CK but not lactate could be used to differentiate patients who later developed subtle mental changes. Although CPB appeared to induce metabolic changes in the brain that could possibly disturb function, severe cerebral damage appeared to require additional global or focal anoxic-ischemic factors. Short hypothermia during bypass did not influence CK, but it was falsely elevated after prolonged hypothermic periods. The testing of these enzymes may be a reliable indicator of the degree of brain damage and the prognosis.
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PMID:Temporal pattern of enzyme changes in cerebrospinal fluid in patients with neurologic complications after open heart surgery. 360 28

I assessed the effect of therapeutic hypothermia on the activity in cerebrospinal fluid of creatine kinase (EC 2.7.3.2) and its brain isoenzyme (CK-BB), lactate dehydrogenase (EC 1.1.1.27), and aspartate aminotransferase (EC 2.6.1.1.) as markers of cerebral damage in patients with transient anoxic-ischemic brain injury. Moderate hypothermia (30-32 degrees C) lasting more than 24 h resulted in disproportionately greater activity of creatine kinase during the post-insult period than in patients not treated with hypothermia but having similar insults and outcome (p less than .01 for survivors, and p less than .005 for nonsurvivors). No differences were observed for the thermostable enzymes lactate dehydrogenase and aspartate aminotransferase, which demonstrates that the effect of hypothermia must be taken into account when thermolabile enzymes are used as sole markers of brain damage in such patients.
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PMID:Effects of therapeutic hypothermia on activity of some enzymes in cerebrospinal fluid of patients with anoxic-ischemic brain injury. 371 42

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.
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PMID:Cardiac enzyme changes in myxedema coma. 382 11

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

Five male rhesus monkeys (Macaca mulatta) were subjected, under ketamine anesthesia, to repeated hypothermia treatments that produced an average rectal temperature of 28.3 degrees C. Following hypothermia induction, the subjects were rewarmed using either a ventrally applied surgical heating pad supplied with 35 degrees C water or a radio-frequency (RF) induction coil operating at 13.56 MHz with an average specific absorption rate (SAR) calculated to be approximately 5.5 W X kg-1. A special temperature probe, nonperturbing to RF, was used in the RF rewarming experiments. Control experiments were also conducted in which only ketamine was administered over a 3-h period. RF rewarming to 35 degrees C typically required only 50 min; whereas, an average of 137 min was required for heating-pad rewarming. Analyses of blood serum collected during and up to 48 h after hypothermia treatments showed elevations at 24 h in creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and glutamic oxaloacetic transaminase (GOT), and these elevations were highest for the ketamine controls and lowest for the RF rewarming experiments. The subjects have been periodically examined since these experiments, and all appear to be in good health. It is concluded that the careful application of RF energy to the central core of the body can successfully be used for rewarming purposes, is more effective than externally applied rewarming techniques, and is potentially useful in remote locations.
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PMID:Hypothermia and electromagnetic rewarming in the rhesus monkey. 651 17

The effects of adenosine on the acute toxicity and oncolytic activity of adriamycin (ADR) were evaluated in mice. When administered as a single i.p. injection of 17.5 mg/kg, adriamycin produced death in all mice within 12 days after treatment, with a mean survival time of 5-9 days. In contrast, the mean survival time of mice administered adenosine subcutaneously (200 mg/kg) in addition to adriamycin was significantly increased compared to adriamycin-treated mice. The protection elicited by adenosine was apparently not a generalized phenomenon of purines, however, since neither hypoxanthine nor inosine were effective protectants. Although a number of adenosine treatment schedules were tested, it was found that adenosine given immediately after adriamycin was as effective as multiple adenosine injections. Administration of adenosine had no apparent effect on adriamycin-mediated changes in ventricular weight, leukocyte count, elevated serum lactic dehydrogenase (LDH) activity or in the histopathologic changes observed in selected tissues. Two grossly observable effects of adenosine administration were lethargy and peripheral hypothermia, which were first noticed approximately 15 min after adenosine administration and which lasted for up to 2 hr. Finally, adenosine had no adverse effect on the antitumor efficacy of adriamycin against L1210 ascites cells inoculated i.p. to BDF1 mice.
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PMID:Reduction of acute adriamycin toxicity in mice treated with adenosine. 668 57


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