Effects of diazoxide on the mitochondrial ultrastructure and permeability in donor rat myocardium.
- Author:
Pei-lin HU
1
;
Ming-zhi ZHENG
;
Jian-ping JIANG
;
Wen-liang CHEN
;
Ying-ying CHEN
;
Yue-liang SHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cryopreservation; Diazoxide; pharmacology; Heart; In Vitro Techniques; Male; Mitochondria, Heart; physiology; ultrastructure; Mitochondrial Membrane Transport Proteins; drug effects; metabolism; Organ Preservation Solutions; pharmacology; Potassium Channels; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2010;26(1):19-22
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of diazoxide (DE) on the myocardial ultrastructure and opening of maitochondrial permeability transition pore (MPTP) in donor rat heart suffered from long-term hypothermic preservation.
METHODSThe Langendorff model of isolated rat heart was used. The hearts were stored in 4 degrees C Celsior solution containing different concentration of DE (15, 30, or 45 micromol/L) for 9 h followed by 60 min of reperfusion. The recovery of rate-pressure product (RPP) was observed. The opening of MPTP and myocardial mitochondria ultrastructure were also evaluated.
RESULTS(1) As compared with the celsior solution preserved group, DE (30 micromol/L) increased recovery of RPP during reperfusion and inhibited the opening of MPTP. DE also alleviated the myocardial mitochondrial ultrastucture damage induced by long-term hypothermic preservation. (2) The above effects of DE were attenuated by a mitoK(ATP) channel inhibitor 5-hydroxydecanoate and a MPTP opener atractyloside.
CONCLUSIONIn the donor rat heart, DE protects myocardial mitochondria ultrastructure against long-term hypothermic preservation injury via inhibiting the opening of MPIP.
