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

To assess the effects of body temperature on renal susceptibility to ischemic injury, rats were rendered acutely hypothermic (90-93 degrees F), normothermic (98-99 degrees F), or hyperthermic (101-103 degrees F) with a heat-controlled surgical board and then were subjected to 25 min of bilateral renal artery occlusion (RAO). Renal high-energy phosphates, their degradation products, and nonprotein sulfhydryl (NPSH) content were assessed at selected times during the peri-ischemic period. The severity of acute renal failure (ARF) was determined for 48 h following RAO by blood urea nitrogen (BUN) and plasma creatinine determinations and by renal histology. Ischemic ATP, ADP, AMP, GTP, GDP, UTP, and NAD levels and postischemic NPSH levels (15 min reflow) inversely correlated with temperature (P less than 0.001). BUN, creatinine concentrations (at 24 and 48 h), and histological injury (at 48 h) directly correlated with temperature (P less than 0.01). Hyperthermia in the absence of RAO had no demonstrable adverse renal effects. We conclude that hyperthermia potentiates ischemic renal injury, whereas hypothermia confers protection. These effects are associated with, and may be influenced by, temperature-induced changes in renal high-energy phosphate availability and oxidant stress during the ischemic/postischemic period.
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PMID:Body temperature: an important determinant of severity of ischemic renal injury. 372 86

A number of hemostasis parameters were studied in a total of 63 patients undergoing cardiopulmonary bypass (CPB) for open heart surgery. In 33 patients fibrinogen, Factors II, V, VIII:C, X, XI, antithrombin, plasminogen, alpha 2-antiplasmin, and platelet counts were assayed before surgery, during maximal hypothermia, at the end of the bypass procedure, before and after protamine sulfate infusion, in the intensive care unit, and 48 hours postoperatively. All factors assayed decreased markedly when the patients were placed on the bypass machine, the drop fairly well paralleling the decrease in hematocrit. During bypass the factors remained low, although a slight tendency toward an increase was noted. Only platelet counts remained low with a decreasing trend until the end of bypass. In the intensive care unit a second decrease in fibrinogen, Factors II and V and antithrombin was noted. This drop was unrelated to four patients who experienced a greater blood loss during this time than the others. Forty-eight hours postoperatively, a marked increase could be found in all clotting factors and near normal levels were measured. Platelet counts remained low, however. The decrease in factors rarely dropped into a range where one would expect a compromised hemostasis (less than 30%). Although antithrombin levels decreased below 60%, no difficulties with heparinization were encountered. Several factors were assayed manually and by automated analyzer (Multistat III), and excellent correlations were found between both procedures. Also a good correlation was found between the activated whole blood clotting times and quantitative heparin assays. In 30 additional patients platelet function was studied before surgery, after thoracotomy, after heparin administration, after initiation of bypass, at maximal hypothermia, before and after protamine sulfate infusion, and 24 hours postoperatively. Platelet counts once again decreased as patients were placed on the CPB machine and remained low throughout the procedure. Mean platelet volumes were unchanged until protamine was given. At that time, a significant drop in mean platelet volume was recorded. Twenty-four hours postoperatively the volumes were normal again. Platelet aggregation studies were performed on a whole blood aggregometer using two concentrations of ADP, collagen, and ristocetin as aggregation inducers. A significant decrease in aggregability was seen when the patients were connected to the CPB apparatus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hemostasis changes during cardiopulmonary bypass surgery. 404 52

Short-lasting hypothermia during thiobutabarbital general anaesthesia causes no decrease of the absolute ATP level in the blood and liver of rats. The adenylate energy charge in the tissues is relatively high - 0.86 in the liver and 0.85 in the muscles, which might be an evidence of a significant "energy sparing" during moderate hypothermia (26 +/- 1 degree C). Somatostatin in a dose of 20 micrograms/kg of body weight given to the rats during hypothermia decreased the ATP level, the ATP/ADP ratio and the adenylate energy charge in the studied tissues, especially in the liver, evidencing increased intensity of catabolic processes caused by the inhibitory action of somatostatin on the release of insulin and glucagon, among other hormones, and on the change of the insulin/glucagon ratio.
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PMID:Somatostatin effect on the level of adenyl nucleotides in the blood and tissues of rats during short-lasting hypothermia. 614 95

It is shown that the amount of ATP in rats under hypothermia up to heat stroke lowers and that of ADP and AMP somewhat rises. Ionol administration normalizes the ATP level and increases the ADP and AMP contents. Inhalation of CO2 and especially administration of ionol contribute to a higher resistance of the animals to hyperthermia.
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PMID:[Influence of hyperthermia and protective effect of ionol and carbon dioxide gas on ATP, ADP and AMP content of the rat brain]. 678 22

Administered intracisternally, adenosine (ADO), 2-chloroadenosine (CADO), adenosine-5'-cyclopropylcarboxamide (ACC) and adenosine-5'-ethylcarboxamide (AEC) caused dose-related increases in hot plate reaction times in mice. The rank order of potency was AEC=ACC greater than CADO greater than ADO and ACC exerted demonstrable effects with doses as low as 10 ng/mouse. ADO itself was more potent than AMP, ADP, ATP and several other related compounds of interest. Theophylline, caffeine and 8-phenyltheophylline antagonized the antinocisponsive effect of CADO or ACC. Papaverine (an adenosine uptake blocker) and erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA: an adenosine deaminase inhibitor) potentiated the effect of ADO. EHNA did not potentiate the action of CADO in this procedure. The antinocisponsive effect of CADO was not antagonized by a host of neurally active agents including naloxone, clonidine and RO 20-1724. Time course studies indicated that the antinocisponsive effect of ADO was transient with the peak effect occurring 5 min after injection and disappearing by 60 min, whereas the effect of CADO persisted for at least 90 min. Intracisternally administered CADO also caused a pronounced hypothermia, loss of muscle tone and was active in the mouse writhing test. Taken together, these data demonstrate that purine exert potent in vivo behavioral effects and are consonant with the existence of a central purinergic P1-receptor which is amenable to selective pharmacological manipulation.
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PMID:In vivo behavioral assessment of central nervous system purinergic receptors. 689 75

Twelve anesthetized mongrel dogs were subjected to systemic hypothermia and potassium-induced cardioplegia for 60 minutes with or without magnesium-1-aspartate. The effect of magnesium was assessed by indices of mitochondrial oxidative phosphorylation. Cardiac arrest was induced by potassium (20 mEq per liter) (6 dogs) or potassium (20 mEq per liter)- magnesium (8 mM per liter). The heart was reperfused for ten minutes following arrest. Dogs were supported by standard cardiopulmonary bypass with hypothermia at 20 degrees C of myocardial temperature. Mitochondria were isolated from the endocardium, the epicardium of the left ventricle and the ventricular septum. ADP: 0 ratio and state 3 respiration were well maintained in both groups following 60 minutes of ischemic arrest and 10 minutes of reperfusion. Magnesium suppressed the non-phosphorylated oxygen consumption of mitochondria, therefore, respiratory control index was signficantly enhanced in the group of potassium-magnesium-1-aspartate cardioplegia. These data suggest that magnesium protects functional capacity of mitochondrial phosphorylation in the myocardium from ischemia.
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PMID:Effect of magnesium in cardioplegic solution upon hypothermic ischemic myocardial mitochondria. 736 86

Hypothermic cardiopulmonary bypass (CPB) has been associated with both coagulation defects and hemorrhage. The influence of temperature on platelet function and the benefits of aprotinin in this situation were studied in 60 patients undergoing elective aortocoronary bypass grafting. The patients were randomly divided into four groups (15 patients per group): group 1, normothermic CPB (nasopharyngeal temperature > 34 degrees C); group 2, normothermic bypass and administration of high-dose aprotinin (2 million IU before CPB, 500,000 IU/h until the end of the operation, and 2 million IU added to the prime); group 3, hypothermic CPB (nasopharyngeal temperature < 28 degrees C); and group 4, hypothermic CPB and aprotinin. Platelet function was evaluated by aggregometry (turbidimetric technique), and aggregation was induced by adenosine diphosphate (1 and 2 mumol/L), collagen (4 micrograms/L), and epinephrine (25 mumol/L) before, during, and after CPB into the first postoperative day. Starting from comparable baseline values, maximum platelet aggregation and maximum gradient of platelet aggregation were significantly most reduced after CPB in group 3 (hypothermic CPB without aprotinin) (ranging from -30% to -53% relative to baseline values). In comparison with the other groups, platelet function in this group also recovered less quickly in the later post-bypass period. Hypothermic CPB with aprotinin resulted in less-altered platelet function than hypothermic CPB without aprotinin. Platelet aggregation in aprotinin-treated patients was comparable overall with that in patients undergoing normothermic CPB. On the first postoperative day, aggregation variables had returned to or exceeded baseline values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet function in cardiac surgery: influence of temperature and aprotinin. 750 60

The current study was undertaken so that the effects of both ischemia and ischemia + hypothermia could be examined in mammalian liver. Particular reference was made to the function of glycolysis, which is the only mechanism for energy production under these conditions. The response of adenylate pools reflected the energy imbalance created during warm ischemia within minutes of organ isolation. ATP levels and energy charge values for control (freshly isolated) livers were 1.20 +/- 0.07 and 0.49 +/- 0.02 mumol/g. Within 5 min of warm ischemia, ATP levels had dropped well below control values and by 30 min warm ischemia, ATP, AMP, and E.C. values were 0.21, 2.01, and 0.17 mumol/g, respectively. Cold ischemic livers (flushed with Marshall's citrate solution and stored on ice) exhibited similar, but more protracted, patterns of adenylate depletion (ATP and ADP) and accumulation (AMP). In both warm and cold ischemic livers, levels of fructose-6-phosphate (F6P) and fructose-1,6-bisphosphate (F1,6P2) indicated a marked activation of glycolysis at the phosphofructokinase (PFK) locus after a certain time of ischemia. Although the activations occurred at different times (30 min and 10 h for warm and cold ischemic livers, respectively), the patterns of change in levels of glycolytic metabolites associated with the PFK-catalyzed reaction were similar; levels of F6P dropped and F1,6P2 increased. Changes in metabolite levels (phosphoenol pyruvate and pyruvate) associated with another key suspect regulatory enzyme, pyruvate kinase, indicated no role in regulatory control of glycolysis during warm or cold ischemia. The activation of PFK at 30 min and 10 h of warm and cold ischemia, respectively, may reflect the accumulating effects of loss of intracellular homeostasis, which leads to impending irreversible damage.
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PMID:Glycolysis and energy metabolism in rat liver during warm and cold ischemia: evidence of an activation of the regulatory enzyme phosphofructokinase. 798 53

We evaluated cerebral metabolism during retrograde cerebral perfusion (RCP) and circulatory arrest during profound hypothermia, and also investigated the effects of perfusion pressure on RCP. Twenty-four adult mongrel dogs were placed on cardiopulmonary bypass and cooled to a nasopharyngeal temperature of 20 degrees C. At this temperature, hypothermic circulatory arrest (HCA; n = 6), and RCP with a perfusion pressure of 10 mmHg (RCP10; n = 6), 20 mmHg (RCP20; n = 6), and 30 mmHg (RCP30; n = 6) were carried out for 60 minutes. RCP was performed with oxygenated blood via the bilateral maxillary veins, and the retrograde flow rate was regulated to maintain a mean perfusion pressure of 10, 20, or 30 mmHg in the external jugular vein. At 60 minutes of RCP, we measured nasopharyngeal temperature; regional cerebral blood flow (rCBF); cerebral oxygen consumption, carbon dioxide excretion, and excess lactate; cerebral tissue adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and energy charge; and cerebral tissue water content. In the RCP10 group, there was excess cerebral lactate, and ATP and energy charge were low. In the RCP30 group, the water content of cerebral tissue was significantly higher than in other groups. In the RCP20 group, temperature was maintained in a narrow range, oxygen consumption and carbon dioxide excretion could be observed, there was no excess lactate, and ATP and energy charge were significantly higher than in the HCA group. In conclusion, RCP can provide adequate metabolic support for the brain during circulatory arrest, and a perfusion pressure of 20 mmHg is most appropriate for RCP.
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PMID:Optimal perfusion pressure for experimental retrograde cerebral perfusion. 799 97

The effects of cold and restraint and of some of the antiulcer drugs on adenosine nucleotide content in the gastric glandular mucosa were examined. A bioluminescence technique was used to measure the amount of ATP and its metabolites in gastric mucosal tissue. Cold-restraint produced gastric lesions and increased the gastric mucosal ATP. Verapamil pretreatment attenuated these lesions and further intensified the ATP increase in a dose-related manner. The ATP/ADP ratio and the Atkinson index were also elevated. Calcium gluconate produced similar effects. Atropine or EGTA pretreatment protected or worsened the gastric lesion, respectively, but did not have any influence on the changes in mucosal energy metabolism. Ranitidine pretreatment lessened the lesion formation but had no influence on the nucleotide content. These findings indicate that the metabolic rate of the gastric mucosa is suppressed during cold-restraint conditions; this depression is probably due to hypothermia and reduction of mucosal metabolism. The lesion-protecting mechanisms of the drugs do not seem to be mediated through their effects on mucosal energy metabolism. The oxygen- and ATP-sparing effects of verapamil may contribute partly to its gastro-protective effect.
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PMID:Role of gastric glandular mucosal energy metabolism in cold-restraint gastric lesion formation. 818 16


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