Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were kept in barochamber for 2 hours at the pressure of 240 mm Hg after subcutaneous administration of (1)14C-acetate. Hypobaric hypoxia caused depression in the incorporation of labeled acetate similar in both phospholipid (PL) components. But the dependence of depression in the metabolic rate upon hypothermia which accompanied hypoxia was more pronounced for hydrophobic portion of PB (carbon skeleton of fatty acids) than for hydrophilic one. Similarity in the degree of the hypoxia induced depression of incorporation of the precursors containing labeled phosphorus and carbon allows one to suggest that the carbon-containing parts of PL hydrophilic components (glycerol and nitrogen bases) and residues of ortho-phosphoric acid respond to hypoxia as a whole.
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PMID:[Effect of hypobaric hypoxia on the acetate-1-14C incorporation rate in hydrophilic and hydrophobic brain phospholipid components]. 51 97

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

The clinical course of 42 children with intracranial pressure monitoring was reviewed. Intracranial hypertension was documented in a variety of diagnostic categories. Therapy was titrated to maintain a baseline intracranial pressure of less than 15 torr (mm Hg), and to decrease the frequency of spontaneous and reactive pressure waves. Ventricular drainage, controlled hyperventilation, intravenous glycerol osmotherapy, therapeutic hypothermia, and barbiturate loading were employed as needed to achieve those goals. Survival was significantly related to average and peak intracranial pressure levels and to the degree of serum hyperosmolality that developed during therapy.
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PMID:Intracranial pressure: monitoring and normalization therapy in children. 85 Jun

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 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

Mice given propylthiouracil, a thyroid inhibitor, and fed a diet containing a nontoxic level of rac-1(3)-palmitoyl glycerol showed the hypothermia and mortality expected for a toxic dose, but did not show these signs when linoleate or oleate was added to the diet. Loss of radioiodine from the whole animal and thyroid gland was slower when mice were fed the toxic palmitoyl glycerol diet than when fed the same diet containing 4% safflower oil. However, mice fed the two diets did not differ in the extent of the incorporation of radioiodine, and essentially all was bound to protein in each case. Follicular thyroid cells from mice fed the potentially toxic diet that contained unsaturated fat were normal in appearance. Conversely, cells from mice fed the toxic diet were smaller and more densely stained, showing evidence of glycoprotein inside the cell. These findings show that the thyroid gland is affected by the palmitoyl glycerol diet. However, the thyroid is not the only organ affected, because giving either thyroxine or triiodothyronine had no effect on the toxicity of palmitoyl glycerol.
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PMID:Toxicity of palmitoyl glycerol to mice: depression of thyroid function. 311 86

When a diet containing 30% rac-1(3)-myristoyl glycerol was fed to mice, they developed hypothermia and death occurred within a few days. If 4% safflower oil was added to the diet containing the myristoyl glycerol, hypothermia did not develop and the mortality decreased. There was a pronounced effect of ambient temperature on the toxic effects of rac-1(3)-myristoyl glycerol. Overall, the effects of feeding rac-1(3)-myristoyl glycerol paralleled the previous findings with rac-1(3)-palmitoyl glycerol. Thus there is a general toxicity associated with feeding the monoacylglycerol of any saturated fatty acid that can be reversed by including small amounts of safflower oil in the diet. The only change in plasma lipids that appears to be relevant to the toxicity and its reversal by safflower oil is an increase in cholesteryl linoleate and a corresponding decrease in the cholesteryl ester of the dietary monoacylglycerol. Even though mice ingested large amounts of rac-1(3)-myristoyl glycerol, the percentage of myristic acid in the plasma lipids was not higher than that found when a fat-free diet was fed, and was not affected by the level of myristoyl glycerol in the diet.
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PMID:Toxicity of rac-1(3)-myristoyl glycerol to mice. 321 75

The goal of this study was to assess the response of fetal brown fat in vivo to hypothermia and norepinephrine infusion. In 10 unanaesthetized, chronically-prepared fetal sheep (133 +/- 2 days of gestation) cold water was passed through tubing encircling the fetus in utero and plasma glycerol concentration was measured as an indicator of brown fat activity. Following cooling for 60 min, amniotic fluid temperature fell 7.79 degrees C to 31.66 +/- 1.73 degrees C (n = 8, P less than 0.001) and maternal temperature fell 0.63 degree C to 38.63 +/- 0.08 degrees C (n = 9, P less than 0.001). Eight of the fetuses were subjected to a second experiment in which norepinephrine was infused intravenously for 15 min. During infusion fetal arterial temperature fell 0.38 degrees C to 39.05 +/- 0.25 degrees C (n = 7, P less than 0.05). Amniotic fluid temperature (n = 7, NS) and maternal arterial temperature (n = 7, NS) remained constant. Glycerol concentration during the infusion increased from 0.73 to 1.27 mg/dl, a 74% increase over control (n = 8, P less than 0.001). Although clearly detectable, these glycerol responses to hypothermia and norepinephrine stimulation are one-third or less of those achieved after birth, indicating that thermogenesis remains quiescent in the near-term fetal sheep, despite powerful stimuli for activation.
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PMID:In vivo brown fat response to hypothermia and norepinephrine in the ovine fetus. 322 Oct 57

Adult and weanling mice kept at low ambient temperatures show an increased sensitivity to the toxicity of dietary rac-1(3)-palmitoyl glycerol. When fed the palmitoyl glycerol, mice less than 6 wk old show a pronounced hypothermia that is prevented by adding safflower oil to the diet. A more moderate degree of hypothermia is seen with older animals. Once body temperature fell below 28 degrees C, replacing the toxic monoacylglycerol with safflower oil and/or raising the environmental temperature to 34 degrees C did not reverse the ultimate fatality caused by palmitoyl glycerol ingestion. If hypothermia was between 28 and 32 degrees C, high mortality was not reversed by feeding the unsaturated fat or raising the environmental temperature to 34 degrees C. However, a combination of both treatments reduced the mortality. Irrespective of body temperature, the hypothermia was eliminated by the warm ambient temperature, but mortality was high. Thus, although hypothermia is a sign of the toxicity of rac-1(3)-palmitoyl glycerol, it is not the immediate cause of death.
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PMID:Toxicity of palmitoyl glycerol to mice: hypothermia and reversal of the toxicity. 366 79


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