Role of mitochondrial calcium uniporter in cardioprotection induced by ischemic postconditioning in isolated rat heart.
- Author:
Tu-nan YU
1
;
Hao HONG
;
Jie-qiong YANG
;
Qin GAO
;
Qiang XIA
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium Channels; metabolism; physiology; Disease Models, Animal; Formazans; analysis; Heart; physiopathology; Ischemic Postconditioning; L-Lactate Dehydrogenase; analysis; Male; Myocardial Reperfusion Injury; metabolism; physiopathology; prevention & control; Rats; Rats, Sprague-Dawley
- From: Journal of Zhejiang University. Medical sciences 2011;40(3):304-308
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of mitochondrial calcium uniporter in cardioprotection elicited by ischemic postconditioning (Postcond).
METHODSMale Sprague-Dawley rats were used for Langendorff isolated heart perfusion. The hearts subjected to global ischemia for 30 min followed by 120 min of reperfusion. Left ventricular developed pressure (LVDP), maximal rise/fall rate of left ventricular pressure (± dP/dtmax) were measured. The level of lactate dehydrogenase (LDH) in the coronary effluent was measured spectrophotometrically, the content of formazan of myocardium was also measured at the end of reperfusion.
RESULTCompared to I/R group, Postcond had an significant increase in the mechanical function of the left ventricle, with LDH release reduced and the content of formazan increased. Spermine, the opener of mitochondrial calcium uniporter, deteriorated the mechanical function of left ventricle and decreased the formazan content, and increased LDH release. Ruthenium red, the inhibitor of mitochondrial calcium uniporter, increased the mechanical function of the left ventricle, decreased the LDH release, but the content of formazan was not increased.
CONCLUSIONThe inhibition of mitochondrial calcium uniporter is involved in the mechanisms of ischemic postconditioning.
