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

We examined the effects of sevoflurane anesthesia with hypothermia on ischemic brain cellular respiration using Wistar strain rats. Ischemia was induced by decapitation. L/P in brain increased during no anesthesia-normothermia-ischemia (1), then gradually, but not fully recovered during 2.5% sevoflurane anesthesia-normothermia-ischemia (2) and during 2.5% sevoflurane anesthesia-hypothermia-ischemia (3). Energy charge decreased during (1) and slight recovery was observed during (3). Respiratory control ratio in brain mitochondria decreased during (1) and recovery during (2) and (3) was slight. No recovery was observed in ADP/O. These findings indicate that during sevoflurane anesthesia with hypothermia, ischemic brain energy metabolism has an effect not on the mitochondrial energy producing processes but on the consuming system.
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PMID:[The effects of sevoflurane anesthesia with hypothermia on ischemic brain cellular respiration]. 823 Jun 90

A number of cardiac metabolic intermediates, namely, adenosine triphosphate (ATP), H+, phosphocreatine (PCr), inorganic phosphate (Pi), adenosine diphosphate (ADP), and related functions of these intermediates, Gibbs' free energy of ATP hydrolysis (delta G) and phosphorylation ratio [ATP/(ADP.Pi)], are thought to adjust mitochondrial oxidative phosphorylation rates to conform to mechanical demand. The effects of hypothermia and altered perfusion pressure on these parameters were evaluated in 12 hearts from Sprague-Dawley rats perfused in the Langendorff mode. 31P-nuclear magnetic resonance (NMR) spectra were obtained at cardiac temperatures between 20 and 37 degrees C, and coronary perfusion pressures between 20 and 145 cm H2O. Coronary flow varied between 0.5 and 15 ml/min throughout this range of intervention. Heart rate (HR), left ventricular systolic pressure (LVSP), and specific volumetric coronary flow (SCF) were determined for each temperature and perfusion pressure. The product HR x LVSP directly correlated with perfusion pressure at all temperatures. The temperature dependence could be represented by an overall activation energy of 72.7 kJ/M. In the constant temperature experiment, SCF and HR x LVSP fell linearly with decreasing perfusion pressure. Quantitative evaluation of the relationship between cardiac function and the metabolic intermediates described above defined these intermediates as nonregulatory with the possible exception of H+.
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PMID:Effect of temperature and coronary flow on the metabolic and mechanical function of the isolated rat heart. 840 50

After O2 deprivation, tissue acidosis rapidly self-corrects. This study assessed the effect of this pH correction on the induction, and pathways, of posthypoxic proximal tubular injury. In addition, ways to prevent the resultant injury were explored. Isolated rat proximal tubular segments (PTSs) were subjected to hypoxia/reoxygenation (50/30 or 30/50 minutes) under the following incubation conditions: 1) continuous pH 7.4, 2) continuous pH 6.8, or 3) hypoxia at pH 6.8 and reoxygenation at pH 7.4 (NaHCO3 or Tris base addition). Continuously oxygenated PTSs maintained under these same pH conditions served as controls. Lethal cell injury was assessed by lactate dehydrogenase (LDH) release. pH effects on several purported pathways of hypoxia/reoxygenation injury were also assessed (ATP depletion, lipid peroxidation, and membrane deacylation). Acidosis blocked hypoxic LDH release (pH 7.4, 50 +/- 2%; pH 6.8, 6 +/- 1%) without mitigating membrane deacylation or ATP depletion. During reoxygenation, minimal LDH was released (3-5%) if pH was held constant. However, if posthypoxic pH was corrected, immediate (< or = 5 minutes) and marked cell death (e.g., 55 +/- 3% with Tris) occurred. This was dissociated from lipid peroxidation or new deacylation, and it was preceded by a depressed ATP/ADP ratio (suggesting an acidosis-associated defect in hypoxic/posthypoxic cell energetics). Realkalinization injury was not inevitable, since it could be substantially blocked by 1) posthypoxic glycine addition, 2) transient posthypoxic hypothermia, or 3) allowing a 10-minute reoxygenation (cell recovery) period before base addition. Neither mannitol nor graded buffer Ca2+ deletion conferred protection. Acute pH correction caused no injury to continuously oxygenated PTSs. Conclusions are as follows: 1) Posthypoxic "pH shock" causes virtually immediate cell death, not by causing de novo injury but, rather, by removing the cytoprotective effect of acidosis. 2) This injury can be prevented by a variety of methods, indicating a great potential for salvaging severely damaged posthypoxic PTSs.
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PMID:Physiological pH. Effects on posthypoxic proximal tubular injury. 844 71

Rewarming from accidental hypothermia is associated with fatal circulatory derangements. To investigate potential pathophysiological mechanisms involved, we examined heart function and metabolism in a rat model rewarmed after 4 h at 15-13 degrees C. Hypothermia resulted in a significant reduction of left ventricular (LV) systolic pressure, cardiac output, and heart rate, whereas stroke volume increased. The maximum rate of LV pressure rise decreased to 191 +/- 28 mmHg/s from a control value of 9,060 +/- 500 mmHg/s. Myocardial tissue content of ATP, ADP, and glycogen was significantly reduced, whereas lactate content remained unchanged. After rewarming, heart rate returned to control value, whereas LV systolic pressure, cardiac output, and stroke volume all remained significantly depressed. The posthypothermic maximum rate of LV pressure rise was 5,966 +/- 1.643 mmHg/s. The posthypothermic myocardial lactate content was significantly increased (to 13.3 +/- 3.2 nmol/mg from control value of 5.7 +/- 1.9 nmol/mg), and ATP and glycogen remained significantly lowered. Creatine phosphate or energy charge did not change significantly during the experiment. The finding of deteriorated myocardial mechanical function and a shift in energy metabolism shows that the heart could be an important target during hypothermia and rewarming in vivo, thus contributing to the development of a posthypothermic circulatory collapse.
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PMID:Experimental hypothermia and rewarming: changes in mechanical function and metabolism of rat hearts. 884 17

The objective of this study was to investigate the effects of single and repeated administration of CP-55,940 [(-)-cis-3-[2-hydroxy-4-(1, 1-dimethylheptyl)-phenyl]-trans-4-(3-hydroxypropyl)cyclohexanol)] on behaviour, energy metabolism and biotransformation. Single intraperitoneal administration to male Sprague-Dawley rats of CP-55,940 (0.4 mg/kg), induced a behavioural response characterized by 'splayed hind limbs', antinociception, hypothermia and a decrease in locomotor activity. Brain and liver mitochondria of the CP-55,940-treated rats exhibited an increase in respiration and no changes in ADP/O and citrate synthase specific activity. Repeated intraperitoneal administration of CP-55,940 (0.4 mg/kg, 11 days) induced behavioural tolerance, disappearance of the increase in the mitochondrial oxygen consumption as well as an increase in the monooxygenase activities and the content of liver microsomal cytochrome P450. Some hepatic metabolizing enzymes of the cytosolic glutathione-centre system were also affected. Previous studies had indicated that the tolerance after chronic administration of CP-55,940 could be due to down-regulation of brain cannabinoid receptors. The present findings demonstrate that the behavioural tolerance occurs together with modified biotransformation activities.
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PMID:Chronic cannabinoid, CP-55,940, administration alters biotransformation in the rat. 890 24

The present study evaluates the influence of cholera toxin and its B-subunit on thermic responses to morphine in the rats. The holotoxin (1 microg/rat) and the B-subunit (5 microg) were administered ICV and three days later rats were challenged ICV with morphine and tested for changes of body temperature. Cholera toxin, but not its B-subunit, modified the time course of the hyperthermic response induced by a low dose of morphine (2.5 microg), converted the hypothermia due to a higher dose of morphine (18 microg) to a consistent hyperthermia and only partially reduced the greater hypothermia induced by 36 microg of morphine. Cholera toxin-induced modifications of thermic responses to morphine were paralleled with a decreased Gs(alpha) immunoreactivity and a reduced ability for the toxin to catalyse the "in vitro" ADP-ribosylation of Gs(alpha) in hypothalamic membranes. In contrast, at the same time when morphine-induced effects on body temperature were assessed, no changes in pertussis toxin-mediated ADP-ribosylation of Gi(alpha)/Go(alpha), or basal adenylate cyclase activity, or binding of mu-opioid receptor selective ligand [3H]-DAMGO were observed in hypothalamic areas from rats treated with cholera toxin. These findings suggest that adaptative events secondary to prolonged activation of Gs(alpha) play a role in the modifications of thermic responses to morphine induced by CTX.
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PMID:Cholera toxin effects on body temperature changes induced by morphine. 907 89

The effect of intravenously administered Ginkbo biloba extract (EGb 761) on the vasospastic response to platelet activation has been assessed using a cutaneous flap preparation in anaesthetized mice. Arterioles of the axillary artery were observed by intravital microscopy, and platelets were activated by topical application of ADP under two steady state conditions: normothermia (37 degrees C) and hypothermia (24 degrees C). Responses of the cutaneous arterioles to stimulation by topical application of a thromboxane agonist (U46619) were also compared in animals treated intravenously with EGb 761 or with a thromboxane synthesis inhibitor (U63557). ADP induced a 34% constriction of the arterioles in control animals. However, no arteriolar constriction occurred in response to ADP in platelet-depleted animals (collagen-induced thrombocytopenia) or in animals treated with EGb 761 (60 mg/kg, i.v.). Exposure of the arterioles to hypothermia (24 degrees C) for 10 min induced constriction of 7-12% in all experimental groups of animals. Under these hypothermic conditions, either EGb 761 or thrombocytopenia abolished ADP-induced arteriolar constriction which was substituted by arteriolar dilation, indicating that EGb 761 can inhibit the vasospasm that is produced by platelet activation. As topically applied U46619 (10(-5) M) induced arterioles constriction (about 22%) that was abolished by intravenous treatment with EGb 761, the extract appears to act directly rather than as a thromboxane synthase inhibitor. Collectively, these findings indicate that platelet factors can play a significant role in cutaneous vasospasm, and that EGb 761, via an action on the thromboxane pathway, could be useful in treating Raynaud's phenomenon and other vascular disorders which involve increased thromboxane production.
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PMID:Effect of Ginkgo biloba extract (EGb 761) on the vasospastic response of mouse cutaneous arterioles to platelet activation. 925 82

Spontaneous EDTA-independent cold platelet agglutination is a rare phenomenon that produces pseudothrombocytopenia when blood samples are analyzed in automated cell counters. We report a case of platelet cold agglutinins and an analysis by flow cytometry. A 49 year old woman presented with abnormal vaginal bleed secondary to uterine fibroids. Platelet clumping was observed in blood samples taken in EDTA-, heparin- and citrate-containing tubes. In flow cytometric tests, patient serum agglutinated 16% of normal platelets at 22 degrees C, and 7% of platelets after incubation at 37 degrees C; in contrast, 3% and < 1% of platelets were agglutinated at 22 and 37 degrees C, respectively, after incubation with normal serum. Minimal agglutination (< 10%) was observed with patient serum at a titre of 1:5 or at temperatures > 30 degrees C. After incubation at 4 degrees C, IgM antibody and C3 were increased on the patient's platelets; no significant amount of IgM or C3 was detected on normal platelets. The specificity of the platelet cold agglutinin was determined by competitive inhibition by monoclonal anti-CD41(GPIIbIIIa). Before the addition of monoclonal antibody, patient's serum agglutinated 16% of normal platelets at 22 degrees C; after addition of anti-CD41 only 2% of the platelets were agglutinated. This blocking effect was not observed with anti-CD42. The patient's platelets functioned normally as determined by CD62 and CD63 expression in response to thrombin, normal platelet aggregation in response to collagen, ADP, and ristocetin, and a normal template bleeding time. In summary, platelet agglutination by a platelet cold agglutinin was quantitated by flow cytometry, the responsible antibody was characterized as a low titre IgM with minimal activity > 30 degrees C, and competitive binding studies supported the GPIIbIIIa complex as the binding site for the antibody. Since the antibody did not affect platelet function, we believe that these patients will not suffer complications from their platelet cold agglutinin, but it could pose a problem under circumstances such as cardiac surgery with hypothermia.
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PMID:Platelet cold agglutinins: a flow cytometric analysis. 1035 Nov 32

It is well established that ADP is an important regulator of the oxidative phosphorylation in the mitochondria. Thus, by means of noninvasive techniques it is demonstrated that the relationship between O(2) consumption of the human gastrocnemius at rest and its temperature is likely determined by at least two factors: 1) the modulation of the rate of the chemical reactions imposed by the "physical" temperature-effect; 2) the influence of temperature-induced ADP concentration changes ( approximately 0.83 microM degrees C(-1)) on oxidative phosphorylation. ADP was assessed by applying the temperature-corrected Lohmann equilibrium equation. PCr and ATP were found to increase, with decreasing temperature (-0.54+/-0.05 and -0.17+/-mM degrees C(-1), respectively), while pH varies following the alpha-stat hypothesis (-0.016+/-0.001 pH degrees C(-1)). These findings should be of value when dealing with muscle physiology in extreme environments or clinical applications of hypothermia.
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PMID:Temperature dependence of human gastrocnemius pH and high-energy phosphate concentration by noninvasive techniques. 1074 39

The aim of this study was to determine the effect of different maternal thermal conditions during transient intrauterine ischemia on the mitochondrial respiratory activities in the immature rat brain. On 17 days of gestation, transient intrauterine ischemia was induced by 30 min of right uterine artery occlusion under hypothermic (33.5-34.5 degrees C, n=6), normothermic (36.5-37.5 degrees C, n=6), and hyperthermic conditions (39.5-40.5 degrees C, n=6). All of the pups were delivered by cesarean section at 21 days of gestation and cerebral neocortical tissue was sampled 1 h after delivery. The mitochondrial respiration was measured polarographically in homogenates. In the ischemic uterine horn, ADP-stimulated respiration of the normothermia and the hyperthermia groups decreased significantly to 73 and 74% of the non-ischemic controls, respectively. Since non-stimulated respiration remained unchanged, the respiratory control ratio (RCR) of the normothermia and the hyperthermia groups decreased significantly to 59 and 54% of the non-ischemic levels, respectively. In contrast, the mitochondrial respiratory activities of the hypothermia group showed no differences between the non-ischemic and the ischemic uterine horns. The results demonstrate that mild maternal hypothermia ameliorates the cerebral mitochondrial dysfunction in neonatal rats after intrauterine ischemia due to transient uterine artery occlusion and suggest that maternal thermal conditions, particularly during uteroplacental insufficiency, have important implications for the neuropathological outcome of the newborn.
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PMID:Influence of mild hypothermia on delayed mitochondrial dysfunction after transient intrauterine ischemia in the immature rat brain. 1135 56


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