Changes of myocardial membrane gene expression of natrium pump isoforms in rat with myocardial ischemia reperfusion injury
- VernacularTitle:大鼠心肌缺血再灌注损伤对心肌细胞膜钠泵表达的影响
- Author:
Yongsheng KE
;
Yuefeng CHU
;
Guohua YU
;
Hao YANG
- Publication Type:Journal Article
- Keywords:
endoxin;
ischemia reperfusion injury;
myocardium;
Na+-K+ exchanging ATPase/isoforms;
immunohistochemical assay
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2000;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: Changes of endoxin level, ATPase activities, intramitochondrial Ca2+ concentration, and gene expression of Na+-K+-ATPase isoforms in myocardium of rats with MIR and effect of verapamil were observed, in order to investigate mechanism of endoxin mediating intracellular calcium overload of myocytes. METHODS: Twenty four male Sprauge Dawley rats were randomized into 3 groups. Sham operation group: silk suture was threaded the left anterior descending coronary artery without ligature; MIR group (MIR): left anterior descending coronary artery was subjected to 30 min ligation followed by 45 min reperfusion; verapamil group: MIR model was given 5 mg/kg verapamil. Verapamil was injected via femoral vein 5 min before reperfusion. Left ventricle myocardium samples were processed immediately after reperfusion in order to measure the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase, endoxin level, and intramitochondrial Ca2+ concentration. The levels of ?1, ?2, ?3 and ?1 isoforms of Na+-K+-ATPase were measured by immunohistochemical assay. RESULTS: After MIR, the level of endoxin in myocardium was substantially increased; the activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase in myocardial membrane were significantly decreased while the concentration of intramitochondrial Ca2+ was increased; the levels of the ?1, ?2, ?3 and ?1 isoforms of Na+-K+-ATPase were reduced markedly. Verapamil had only effect on reducing the concentration of intramitochondrial Ca2+. CONCLUSION: MIR increases endoxin secretion. The latter may depress the activity of Na+-K+-ATPase by changing the gene expression of ?1, ?2, ?3 and ?1 isoforms of Na+-K+-ATPase in myocardial membrane, inducing intramitochondrial Ca2+ overload.
