title: Ischemia hypothermia improved contractility under normothermia reperfusion in the model of cultured cardiomyocyte.
abstract: Though mild hypothermia displays an optimistic alleviation of contractive failure in the ischemia/reperfusion myocardium, we still lacked answers to many questions about its potential mechanisms. Our hypothesis is that hypothermia (32°C) induced in ischemia can ease mitochondrial injury resulting in improvement of myocardial contractility even under the condition of a normothermic reperfusion. Fifty newly born 1-2 d Sprague-Dawley rats were executed and the primary cardiomyocytes were obtained and cultivated in vitro. Myocytes were randomized into three groups and then subjected to ischemia either at 32°C or 37°C, both prior to undergoing reperfusion at 37°C. Contractility was presented as frequency and velocity. Ultrastructural alterations of cardiomyocytes and mitochondrion underwent semi-quantitative analysis with transmission electron microscopy and respiratory function of mitochondria was further assessed simultaneously. During cooling ischemia and following reperfusion, cardiomyocytes acquired a more immediate restoration to baseline level and had a significant difference as compared with those in normothermia (P < 0.05). Furthermore, hypothermia preserved the ultrastructure of myocytes and mitochondrion after ischemia. However, measurement on Heart Injury Score and form factor revealed no differences after 2-h reperfusion either in hypothermia or normothermia. On the contrary, the surface area and respiratory function of mitochondrion in reperfusion differed significantly in both groups (P < 0.05) which had an accordance with the variation on contractile performance. Hypothermia only induced in ischemia can bring contractility benefit even under a normothermia reperfusion in cultured cardiomyocytes.
authors.affiliation: Emergency Department, Sun-Yat-Sen Memorial Hospital, Guangzhou, People's Republic of China.
authors.forename: Heng
authors.initials: H
authors.lastname: Li
authors.forename: Xiangshao
authors.initials: X
authors.lastname: Fang
authors.forename: Zhengfei
authors.initials: Z
authors.lastname: Yang
authors.forename: Yue
authors.initials: Y
authors.lastname: Fu
authors.forename: Yu
authors.initials: Y
authors.lastname: Wang
authors.forename: Jinlang
authors.initials: J
authors.lastname: Wu
authors.forename: Tao
authors.initials: T
authors.lastname: Yu
authors.forename: Zitong
authors.initials: Z
authors.lastname: Huang
mesh_terms: D000818:Animals; D019069:Cell Respiration / Q000502:physiology*; D002478:Cells, Cultured; D005947:Glucose / Q000494:pharmacology; D007036:Hypothermia, Induced; D066298:In Vitro Techniques; D007511:Ischemia / Q000139:chemically induced; D046529:Microscopy, Electron, Transmission; D008929:Mitochondria, Heart / Q000502:physiology / Q000648:ultrastructure*; D009200:Myocardial Contraction / Q000502:physiology*; D032383:Myocytes, Cardiac / Q000502:physiology / Q000648:ultrastructure; D010100:Oxygen / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015424:Reperfusion
chemical_list: D005947:Glucose; D010100:Oxygen