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Mechanisms of cardioprotective effects of high concentration of magnesium on hypoxia/reoxygenation injury in chronic magnesium deficient rat heart are differ from normal rat heart (LB665)
Author(s) -
Watanabe Makino,
Nakamura Kyoko,
Kato Megumi,
Kakigi Ryo,
Iesaki Takafumi,
Okada Takao
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb665
Subject(s) - hypoxia (environmental) , mitochondrial permeability transition pore , mptp , magnesium , mitochondrion , extracellular , chemistry , medicine , perfusion , endocrinology , pharmacology , biochemistry , oxygen , apoptosis , programmed cell death , organic chemistry , dopaminergic , dopamine
Magnesium (Mg) deficiency has been reported to be associated with the development of cardiovascular diseases. We have reported that high concentration (12 mM) of extracellular Mg during hypoxia (high‐Mg) protected the heart from hypoxia/reoxygenation (H/R) injury, and its protective effect was induced not only by suppression of energy consumption, but also by opening of mitochondrial K ATP channel in cardiomyocytes. The aim of this study was to determine whether high‐Mg could protect the H/R injury in chronic Mg‐deficient (Mg‐def) rat heart. Rats were fed an Mg‐def diet for 8 weeks, and the hearts were subjected to Langendorff perfusion with the protocol of 30 min hypoxia followed by 30 min reoxygenation. In Mg‐def group, the recovery of cardiac function (pressure‐rate product; PRP) from H/R injury was significantly impaired than that of control group. Recovery of PRP in Mg‐def group was restored to that of control group when extracellular Mg concentration was increased from 1.2 to 12 mM during hypoxia. A specific mitochondrial K ATP channel blocker, 5‐hydroxy decanoic acid (5‐HD), did not inhibit the protective effect of high‐Mg in Mg‐def group. In isolated myocardial mitochondria from Mg‐def rat hearts, retention of Ca 2+ to open the mitochondrial permeability transition pore (mPTP) was significantly lower than that of control group. These results suggest that the mechanisms of cardioprotective effects of high‐Mg do not depend on opening the mitochondrial K ATP channel but on unknown other mechanisms, although the mitochondrial functions are impaired in Mg‐def rat hearts. Grant Funding Source : Supported by JSPS KAKENHI Grant Number 24614015