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)

The effect of pentobarbital on the induction of heat shock protein (HSP) 70 and heat shock cognate protein (HSC) 70 mRNAs after transient global ischemia in gerbil brains was investigated by in situ hybridization using cloned cDNA probes selective for each mRNA species. In sham control brains, HSP70 mRNA was scarcely present, whereas HSC70 mRNA was present in most cell populations. After a 5-min occlusion of bilateral common carotid arteries, HSP70 and HSC70 mRNAs were induced together in several cells and were especially dense in hippocampal dentate granule cells at 3 h, but the strong hybridization of the mRNAs continued only in hippocampal CA1 cells by 2 days. At 7 days after the ischemia, CA1 neuronal cell death was apparent, and the HSP70 mRNA disappeared and HSC70 mRNA content returned to the sham level, except for in the CA1 cells. Pretreatment with pentobarbital (40 mg/kg, i.p.) greatly reduced or inhibited the induction of HSP70 and HSC70 mRNAs at both early (3-h) and late (2-day) phases after ischemia. The drug also prevented CA1 cell death at 7 days along with the maintenance of expression of HSC70 mRNA at the sham control level. Hypothermic effects of pentobarbital were noted at 30 and 60 min after the reperfusion, whereas at 2 h there was no statistical significance between the control and drug-treated groups. The great reduction of HSP70 and HSC70 mRNA induction at both early and late phases after ischemia suggests that pentobarbital reduces intra-and/or postischemic stress and may protect CA1 cells from ischemic damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of HSP70 and HSC70 heat shock mRNA induction by pentobarbital after transient global ischemia in gerbil brain. 851 71

Cardiac surgery is usually performed under conditions of cardioplegic ischemic arrest. To protect the heart during the ischemic period, the myocardium is exposed to varying degrees of hypothermia. Although hyperthermia is known to induce the heat shock response, the molecular effects of hypothermia on the myocardium have not been investigated. We have studied the effect of hypothermia on the induction of heat shock proteins in primary cultures of neonatal cardiomyocytes. Cold stress in cardiomyocytes induced a 6 fold increase in the heat shock protein HSP70 as compared to control. Increased HSP70 protein levels correlated with induction of HSP70 mRNAs. Maximal levels of HSP70 protein appeared 4-6 h following recovery from cold shock, indicating the transient nature of the response. Induction of HSP25 mRNA was also observed in cold-shocked cardiomyocytes, even though increased HSP25 protein levels were not detected. Our results indicate that hypothermia is capable of inducing the heat shock response in neonatal cardiomyocytes.
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PMID:Characterization of cold-induced heat shock protein expression in neonatal rat cardiomyocytes. 927 66

Hypothermia improves resistance to subsequent ischemia in the cardioplegic-arrested heart (CAH). This adaptive process produces mRNA elevation for heat shock protein (HSP) 70-1 and mitochondrial proteins, adenine nucleotide translocator (ANT(1)), and beta-F(1)-ATPase. Glucose in cardioplegia also enhances myocardial protection. These processes might be linked to reduced ATP depletion. To assess for synergism between these protective processes, isolated rabbit hearts (n = 91) were perfused at 37 degrees C and exposed to ischemic cardioplegic arrest for 2 h. Hearts were in four groups: control (C), hypothermia adapted (H) perfused to 31 degrees C 20 min before ischemia, 22 mM glucose (G) in cardioplegia, and hypothermic adaptation and glucose (HG). Developed pressure (DP), dP/dt(max), and pressure-rate product (PRP) improved (P < 0.05) in G, H, and HG compared with C during reperfusion. DP and PRP were elevated in HG over H and G. ATP was higher in G, H, and HG, although no additional increase in HG over H was found. Lactate and CO(2) production were elevated in G only. The mRNA expression for HSP70-1, ANT(1), and beta-F(1)-ATPase was elevated severalfold in H and HG, but not G over C during reperfusion. In conclusion, glucose provides additional functional improvement in H. Additionally, neither ATP levels nor anaerobic metabolism are linked to mRNA expression for HSP70, ANT(1), or beta-F(1)-ATPase in CAH.
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PMID:Mitochondrial protein and HSP70 signaling after ischemia in hypothermic-adapted hearts augmented with glucose. 1040 52

The influence of deep hypothermia (4 degrees C) during a substrate-free, hypoxia-reoxygenation treatment was investigated on cardiomyocytes (CM) prepared from newborn rat heart in culture in an in vitro, substrate-free model of ischemia-reperfusion. The transmembranous potentials were recorded with standard microelectrodes. The contractions were monitored photometrically. The RNA messenger (mRNA) and protein expression for protein (HSP70) were analysed by RT-PCR (reverse transcriptase-polymerase chain reaction) and Western blotting, respectively. Simulated ischemia (SI) caused a gradual decrease and then a cessation of the spontaneous electromechanical activity. During the reoxygenation, the CM recovered normal function, provided that SI did not exceed 2.5 h. When SI duration was increased up to 4 h, reoxygenation failed to restore the spontaneous electromechanical activity. Conversely, the exposure of the CM to SI together with deep hypothermia decreased the functional alterations observed, and provided a complete electromechanical recovery after 2.5 h as well as after 4 h of SI. Deep hypothermia alone failed to induce HSP70 mRNA and protein production. On the contrary, HSP70 mRNA production increased after 2.5 and 4 h of deep hypothermia followed by 1 h of rewarming, proportionally to the duration of the cooling period. This augmentation in mRNA was associated with a rise in HSP70 protein content. In summary, it appeared that deep hypothermia exerts a strong cytoprotective action during SI only, whereas cooling CM before SI has no beneficial effect on subsequent SI. Moreover, these results suggested the persistence of a signaling system and/or transduction in deeply cooled, functionally depressed cells. Finally, CM in culture appeared to be a model of interest for studying heart graft protection against ischemia-reperfusion and contributed to clarifying the molecular and cellular mechanisms of deep hypothermia on myocardium.
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PMID:Influence of deep hypothermia on the tolerance of the isolated cardiomyocyte to ischemia-reperfusion. 1173 54

The authors sought to determine whether Zn translocation associated with neuronal cell death occurs after transient global ischemia (TGI) in mice, as has been previously shown in rats, and to determine the effect of mild hypothermia on this reaction. To validate the TGI model, carbon-black injection and laser-Doppler flowmetry were compared in three strains of mice (C57BL/6, SV129, and HSP70 transgenic mice) to assess posterior communicating artery (PcomA) development and cortical perfusion. In C57BL/6 mice, optimal results were obtained when subjected to 20-minute TGI. Brain and rectal temperature measurements were compared to monitor hypothermia. Results of TGI were compared in normothermia (NT; 37 degrees C) and mild hypothermia groups (HT; 33 degrees C) by staining with Zn -specific fluorescent dye, -(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) and hematoxylin-eosin 72 hours after reperfusion. The Zn translocation observed in hippocampus CA1, CA2, and Hilus 72 hours after 20 minutes of TGI was significantly reduced by mild hypothermia. The number of degenerating neurons in the HT group was significantly less than in the NT group. Mild hypothermia reduced mortality significantly (7.1% in HT, 42.9% in NT). Results suggest that mild hypothermia may reduce presynaptic Zn release in mice, which protects vulnerable hippocampal neurons from ischemic necrosis. Future studies may further elucidate mechanisms of Zn -induced ischemic injury.
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PMID:Mild hypothermia reduces zinc translocation, neuronal cell death, and mortality after transient global ischemia in mice. 1236 62

The present study shows that anoxic neuronal depolarization or NMDA receptor activation are potent stimuli for inducing spinal neuronal heat shock protein 70 (Hsp70). Spinal hyperthermia, despite its significant glutamate releasing effect, induced only glial Hsp70 upregulation. No significant increase in spinal Hsp70 expression after potassium depolarization was seen. Transient spinal ischemia (6 min) was induced by the inflation of a 2F Fogarty catheter placed into descending thoracic aorta during concurrent hypotension (40 mmHg). To determine the onset of anoxic depolarization extracellular concentration of K+ was measured in the lumbar dorsal horn using a microelectrode. Spinal hyperthermia (42 degrees C) or hypothermia (27 degrees C) was induced using a heat exchanger placed in the paravertebral subcutaneous space overlying Th5-S4 spinal segments. To measure extracellular concentration of glutamate during hyperthermia a loop dialysis catheter was implanted into lumbar intrathecal space. Receptor specific (NMDA, 3 microg) or non-specific (KCl, 10 microl, 1M) neuronal depolarization was induced using previously implanted intrathecal catheters. After ischemia, temperature manipulations or drug injections animals survived for 4 or 24h. Animals were then terminally anesthetized and perfusion fixed for Hsp70 immunohistochemistry. After spinal ischemia or NMDA administration a neuronal Hsp70 expression was seen at 24h. After spinal hyperthermia only glial expression was seen at 4h. Hyperthermia significantly increased CSF glutamate concentration, however, MK-801 (a non-competitive NMDA receptor antagonist) pretreatment failed to block Hsp70 expression. After hypothermia or potassium depolarization only minimal or no Hsp70 expression was seen in glial cells. Exposure of neuronal tissue to a specific stimuli may lead to intervals of increased resistance to subsequent neurotoxic/ischemic insult. The intervening biochemistry of this protection has been attributed to a family of molecules referred to as HSP. In the present study, we demonstrate that short-lasting anoxic depolarization or activation of NMDA receptor are the most potent stimuli for spinal neuronal Hsp70 induction. This effect corresponds with the observed ischemic tolerance state induced by short-lasting preconditioning spinal ischemia.
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PMID:Spinal heat shock protein (70) expression: effect of spinal ischemia, hyperthermia (42 degrees C)/hypothermia (27 degrees C), NMDA receptor activation and potassium evoked depolarization on the induction. 1296 88

The study was carried out in order to observe the protective effects of electroacupuncture (EA) and hypothermia on myocardial ischemic and reperfusion injury in pigs. Blood superoxide dismutase (SOD), malondialdehyde (MDA), creatine phosphokinase (CPK) and its isoenzyme (CK-MB), coronary artery flow (CAF) and myocardial heat-shock protein (HSP) mRNA expression were detected. It was observed that the MDA content increased and SOD activities decreased more significantly in control group compared with EA and EA+ hypothermia groups. CPK and CK-MB were found significantly increased in all three groups, but more remarkable in control group than in EA and EA+ hypothermia groups. HSP70 mRNA expression was found to be more in EA and EA+ hypothermia groups than that in control group 60 min after reperfusion. The results indicated that EA enhance the myocardial protection of hypothermia on ischemia/reperfusion injury. The mechanism may be related to the improvement of antioxidation and increased expression of HSP70 gene.
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PMID:Myocardial protective effects of electroacupuncture and hypothermia on porcine heart after ischemia/reperfusion. 1499 57

We have investigated different signaling molecules that could be activated by temperature acclimation and hypoxia, using an experimental approach consisting in submerging frogs in a water-filled box maintained at 2-4 degrees C at ambient oxygen levels or supplied with 98% N2:2% CO2 for normoxia or hypoxia conditions, respectively. The results obtained showed no significant changes in the expression of heat shock protein 70. The phosphorylation state of AMP-dependent activated protein kinase, the down-stream component of a protein kinase cascade that acts as an intracellular energy sensor, was significantly increased in both experimental conditions, showing higher values in the absence of oxygen. Similarly, the phosphorylation state of one of its known substrates, elongation factor 2, was also increased, consistent with the arrest of protein synthesis. These results point out an important role of this kinase, adjusting the rates of ATP-consuming and ATP-generating pathways, in the survival strategies to hypoxia and hypothermia.
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PMID:Activation of AMP-dependent protein kinase by hypoxia and hypothermia in the liver of frog Rana perezi. 1535 90

The beneficial effects of interventions to control fever in sepsis are controversial. We investigated whether the use of acetaminophen and external cooling is beneficial to control fever in septic shock. We studied 24 fasted, anesthetized, invasively monitored, mechanically ventilated female sheep (27.0 +/- 4.6 kg) that received 0.5 g/kg body weight of feces into the abdominal cavity to induce sepsis. Ringer's lactate (RL) was titrated to maintain pulmonary artery occlusion pressure (PAOP) at baseline levels throughout the experimental period. During the 2 h after the surgical operation, animals were placed in the hypothermia group if their temperature fell below 36.0 degrees C; the other animals were randomized to three groups: high fever (T > 39.0 degrees C), mild fever (37.5 degrees C < T < 38.5 degrees C), and normothermia (36.0 degrees C < T < 37.0 degrees C). The administration of 25 mg/kg acetaminophen every 4 to 6 h combined with external cooling (ice pad) was used to control core temperature in these three groups. The PaO2/FiO2 ratio was higher and blood lactate concentration was lower in the high fever than in the other groups (P < 0.01 and 0.05, respectively). Survival time was longer in the high fever group (25.2 +/- 3.0 h) than in the mild fever (17.7 +/- 3.5 h), normothermia (16.0 +/- 1.9 h), and hypothermia (18.5 +/- 2.5 h) groups (P < 0.05 for all). Plasma heat shock protein (HSP) 70 levels were higher in the two fever groups than in the other groups (P < 0.05). In this clinically relevant septic shock model, the febrile response thus resulted in better respiratory function, lower blood lactate concentration, and prolonged survival time. Antipyretic interventions including acetaminophen and external cooling were associated with lower circulating HSP70 levels. These data challenge the temperature control practices often used routinely in acutely ill patients.
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PMID:Fever control in septic shock: beneficial or harmful? 1589 3

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2 supply and/or malfunctioning O2 extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats (n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15 degrees C, kept at 15 degrees C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by > 50% in response to cooling. O2 consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h (group 2) but recovered to only 60% in those rewarmed after 5 h (group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15 degrees C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2 extraction function well during deep/profound hypothermia, and, despite low CO, O2 supply was not a limiting factor for survival in the present experiments.
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PMID:Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia? 1646 71


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