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)

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

Although inducing mild hypothermia (32 degrees C) in animal models of cardiac arrest with highly attenuated cardiac and neurological injury, the protective effects of hypothermia molecular mechanisms were not fully elucidated, and thus, were examined here on the H9c2 rat ventricular myoblasts that underwent cell loss as well as apoptosis in conditions of simulated ischemia, represented by serum withdrawal plus hypoxia. The H9c2 cells apoptosis was evidenced by flow cytometry-, DNA fragmentation-, and caspase 3 activation-increased apoptotic cells (Annexin-V positive and propidium iodide negative). For the simulated ischemia, both cell loss and apoptosis of these cardiomyoblasts were associated with downregulated small molecular weight proteins (heat shock protein 20, heat shock protein 27, and alphaB-crystallin). Mild hypothermia significantly reduced the ischemia-induced apoptosis, small molecular weight proteins downregulation, and cell viability cut. Conclusively, hypothermia may inhibit simulated ischemia-induced apoptosis in cardiomyocytes by restoring normal small molecular weight proteins expression.
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PMID:Attenuating ischemia-induced H9c2 myoblasts apoptosis by therapeutic hypothermia. 2022 Mar 35

Therapeutic hypothermia (TH) is a promising cardioprotective treatment for cardiac arrest and acute myocardial infarction, but its cytoprotective mechanisms remain unknown. In this study, we developed a murine cardiomyocyte model of ischemia-reperfusion injury to better determine the mechanisms of TH cardioprotection. We hypothesized that TH manipulates Akt, a survival kinase that mediates mitochondrial protection by modulating reactive oxygen species (ROS) and nitric oxide (NO) generation. Cardiomyocytes, isolated from 1- to 2-day-old C57BL6/J mice, were exposed to 90 min simulated ischemia and 3 h reperfusion. For TH, cells were cooled to 32 degrees C during the last 20 min of ischemia and the first hour of reperfusion. Cell viability was evaluated by propidium iodide and lactate dehydrogenase release. ROS production was measured by 6-carboxy-2',7'-dichlorodihydrofluorescein diacetate and mitochondrial membrane potential (DeltaPsim) by 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazoly-carbocyanine iodide (JC-1). Phospho (p)-Akt (Thr308), p-Akt (Ser473), and phosphorylated heat shock protein 27 (p-HSP27) (Ser82) were analyzed by Western blot analysis. TH attenuated reperfusion ROS generation, increased NO, maintained DeltaPsim, and decreased cell death [19.3 + or - 3.3% (n = 11) vs. 44.7 + or - 2.7% (n = 10), P < 0.001]. TH also increased p-Akt during ischemia before reperfusion. TH protection and attenuation of ROS were blocked by the inhibition of Akt and NO synthase but not by a cGMP inhibitor. HSP27, a regulator of Akt, also exhibited increased phosphorylation (Ser82) during ischemia with TH. We conclude that TH cardioprotection is mediated by enhanced Akt/HSP27 phosphorylation and enhanced NO generation, resulting in the attenuation of ROS generation and the maintenance of DeltaPsim following ischemia-reperfusion.
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PMID:Therapeutic hypothermia cardioprotection via Akt- and nitric oxide-mediated attenuation of mitochondrial oxidants. 2038 60