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

The effect of cooling and subsequent rewarming on the tissue respiration of canine hearts was studied during polycomponent ether-oxygen anaesthesia. The tests included the determinations of the activity of the dehydrogenases of the cytrate cycle, the content and activity of chromoproteids, the respiration rate of the mitochondrias on succinate, glutamate and ketoglutarate, the content of glycogen, the activity of the phosphorylases, hexokinase, lactate dehydrogenase, the content of lactate, pyruvate, adenyl nucleotides and creatine phosphate. Significant changes were noted in the content and activity of the above substances, acceleration of mitochondrial respiration, reduced energy regulation of respiration, and decreased amount of the adenyl components. It is suggested that under artificial hypothermia the processes of chromoproteids biosynthesis are enhanced, which results in an increased power of terminal respiration, and conformational rearaangements of the enzymes connected with the membranes occur.
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PMID:[Characteristics of energy metabolism in the myocardium under artificial hypothermia]. 19 79

Twenty experiments were conducted on dogs. The effect of hypothermia of different degree (from 18 to 20 degrees C and from 4 to 6 degrees C) on the carbohydrate metabolism and the extent of solubilization of hepatic enzymes (lactate dehydrogenase, glutamate dehydrogenase, urokaninase, DNA-ase, glucose-6-phosphatase) in prefusion-free preservation of the liver was studied. The preservation efficacy was assessed during the subsequent two-hour normothermic perfusion. A marked solubilization of the enzymes under study followed preservation of the liver at 18--20 degrees C; this indicated the loss of intactness of the cell membranes during the preservation. A moderate expenditure of the glycogen stores in the liver, and of sugar in the perfusate followed preservation of the liver at a temperature of 4--6 degrees C; this suggested an even suppression of hepatic metabolism and the prevalence of normal tissue respiration over glycolysis in the restoration of circulation in the liver.
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PMID:[Effect of hypothermia on metabolism in the liver during its preservation]. 68 13

The measurement of lactate dehydrogenase (LDH) release into perfusates after hypothermic storage was found to be a reliable index of ischemic injury of rabbit kidneys. Kidneys were exposed to warm and cold ischemia for varying periods. Each kidney was perfused before and after storage at simple hypothermia with 25 ml of a modified Collins solution. The venous effuent was collected in 5 ml fractions. Total LDH activity was measured in the first fraction after storage and used as a measure of ischemic tissue damage. It was confirmed that increasing the period of cold ischemia result in significant increases in LDH activity. The release of LDH into perfusates was then used to compare kidney damage after preservation with various fluids. With this method, it was not possible to demonstrate any difference in the extent of tissue damage after preservation with sodium-rich vs. potassium-rich perfusion fluid. Addition of steroids, vitamins and essential amino acids did not prevent or reduce tissue damage, estimated in this way. The effects of adding cryoprotectants to the perfusion fluid varied; LDH release following addition of 5% DMSO was significantly greater, and after addition of 5% glycerol smaller than the release after perfusion with a modified Collins solution alone. Stepwise addition of DMSO up to 20% resulted in serious tissue damage with a large LDH release into the perfusate.
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PMID:LDH release into perfusates of preserved kidneys. 78 32

Myocardial cell vulnerability to phospholipase C (PC-PLC) attack was investigated in three different preparations of rat myocardial cells: triacylglycerol (TG)-loaded, hypothermic/rewarmed and energy depleted myocytes. The attack by PC-PLC was evaluated as PC-PLC induced glycerol output due to the combined action of phospholipase C and intracellular lipases. PC-PLC induced glycerol output was significantly higher (p < 0.05) in all three myocyte preparations, compared to their respective controls. Cell morphology (% rod shaped myocytes) of TG-loaded or hypothermic/rewarmed myocytes was not different from their controls, whereas energy depleted myocytes almost exclusively were rounded up, due to hypercontraction of the myofilaments. Hypothermic/rewarmed and energy depleted myocytes showed a significantly higher release of lactate dehydrogenase (LDH), compared to their controls although the difference was much more pronounced in the latter. Finally, the cellular contents of ATP were maintained both in TG-loaded and hypothermic rewarmed myocytes, while energy depleted myocytes contained only about 25% of the normal ATP level. These results demonstrate that attack from exogenously added phospholipases can occur, not only in seriously damaged cardiac myocytes, but in myocytes with a more subtle damage as well.
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PMID:Myocardial cell vulnerability to exogenous phospholipase attack. 148 Jan 54

The combined action of phosphatidylcholine preferring phospholipase C (PC-PLC) and intracellular lipases has recently been shown to cause glycerol output in energy deprived rat cardiomyocytes. In the present study we examined the effect of hypothermia and rewarming on PC-PLC evoked glycerol output in freshly isolated, calcium-tolerant myocytes. The cells were preincubated for 60 min at hypothermic (5 degrees C) or normothermic (37 degrees C) conditions in Krebs-Henseleit bicarbonate buffer (pH 7.4) supplemented with 1 mM DL-carnitine, 1% B.S.A. and 5 mM glucose. Addition of PC-PLC resulted in a significantly higher (P less than 0.05) output of glycerol in myocytes undergoing rewarming than in myocytes kept constantly at 5 degrees C or 37 degrees C. The values obtained for PC-PLC induced glycerol output (difference in glycerol output between incubations with and without PC-PLC) were 6.77 +/- 2.6 (37 degrees C), 4.54 +/- 1.7 (5 degrees C) and 22.85 +/- 5.9 (5-37 degrees C) nmol/10(6) cells.h. Rewarming in addition caused a significantly higher (P less than 0.05) leakage of lactate dehydrogenase (LDH) from the rewarmed cells as compared to cells at constant temperatures (5 degrees C or 37 degrees C). However, there was no additional effect of PC-PLC on LDH leakage. The elevated PC-PLC induced glycerol output in rewarmed myocytes was not related to a fall in the percentage of rod-shaped cells or a reduced cellular content of ATP, since no differences could be detected between the various myocyte preparations with respect to these parameters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of hypothermia and rewarming on phospholipase C-evoked glycerol output in rat myocardial cells. 163 71

The treatment of hypothermia associated with hemorrhage, exposure, or intraoperative intervention continues to represent a challenge for trauma care teams. An innovative technique for combining microwave heating with continuous temperature monitoring into a feedback-controlled system for blood warming has been developed. The effect of microwave warming on the structure and function of blood was compared with that in nonheated controls. Erythrocyte structural integrity (hemolysis) was evaluated by comparing levels of lactate dehydrogenase (LDH), potassium (K+), and plasma hemoglobin (PHGB), and hematocrit (HCT) in heated and nonheated (control) samples of banked red blood cells. Hemoglobin function was evaluated in fresh blood by comparing the P50 and hemoglobin electrophoresis of experimental and control samples. Prewarming temperatures were 3 degrees or 23 degrees C; temperatures after warming were 35 degrees, 37 degrees, or 39 degrees C. The results reflect the percentage of changes for 84 heated and 24 unheated blood samples. There were no statistical differences in any of the biochemical variables measured. The P50 for three heated and three unheated samples was 30.7 +/- 1.2 and 30.5 +/- 0.9 mm Hg (p greater than 0.05). There were no changes in the hemoglobin electrophoretic patterns in experimental or control samples. This system is designed to deliver microwave energy in a uniform and controlled manner, overcoming the limitations of conventional microwave ovens that in the past caused local overheating and subsequent hemolysis when used for blood warming. The structural and functional integrity of erythrocytes after microwave warming indicate the safety and effectiveness of this technique.
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PMID:The effect of in-line microwave energy on blood: a potential modality for blood warming. 163 11

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


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