COX-2 or nNOS mediates cardioprotection during the final stage of the late phase of ischemic preconditioning.
- Author:
Qing XU
1
;
Bie TANG
;
Ning ZHANG
;
Lihua SONG
;
Zhiqin ZHANG
;
Yingying CHEN
Author Information
1. Basic Medical Experimental Center, Jinhua Vocational and Technological College, Jinhua 321000, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Cyclooxygenase 2;
metabolism;
physiology;
Ischemic Preconditioning, Myocardial;
Male;
Myocardial Infarction;
enzymology;
pathology;
prevention & control;
Myocardial Reperfusion Injury;
enzymology;
metabolism;
prevention & control;
Nitric Oxide Synthase Type I;
metabolism;
physiology;
Rabbits;
Random Allocation;
Time Factors
- From:
Journal of Biomedical Engineering
2008;25(6):1411-1414
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present studies was to investigate the cardioprotection of late IP at 72 h and determine the involvement of iNOS, nNOS and COX-2 in this protection. Conscious rabbits were preconditioned with three cycles of 5-minute coronary occlusion/5-minute reperfusion. The myocardial infarct area in the rabbits preconditioned 72 h earlier was significantly smaller than that in control rabbits. The activity of lactate dehydrogenase (LDH) and the level of 6-Keto-PGF1alpha in the rabbits preconditioned 72 h earlier were lower than those in control rabbits. The left ventricular systolic pressure (LVSP) and maximal velocity of contraction and relaxation (+/- dP/dtmax) were improved in rabbits preconditioned 72 h earlier. The nNOS-selective inhibitors N-propyl-L-arginine and selective cyclooxygenase-2 (COX-2) inhibitor celecoxib completely blocked the protection of late IP at 72 h, whereas the iNOS selective inhibitor S-methybisothiourea had no effect. In conclusion, the cardioprotection observed in the final stage of late IP (72 hours) is mediated by nNOS or COX-2, but not by iNOS.
