Sevoflurane preconditioning produces delayed cardioprotection effect through up-regulation of inducible nitric oxide synthase in rats.
- Author:
Lei-lei MA
1
;
Feng-jiang ZHANG
;
Min YAN
Author Information
- Publication Type:Journal Article
- MeSH: Anesthetics, Inhalation; pharmacology; Animals; Disease Models, Animal; Ischemic Preconditioning, Myocardial; Male; Methyl Ethers; pharmacology; Myocardial Reperfusion Injury; enzymology; pathology; prevention & control; Myocardium; enzymology; pathology; Nitric Oxide Synthase Type II; metabolism; Rats; Rats, Sprague-Dawley; Up-Regulation; drug effects
- From: Journal of Zhejiang University. Medical sciences 2012;41(5):553-558
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether inhaled sevoflurane is capable of producing delayed cardioprotection effect in rats and its underlying mechanisms.
METHODSMale Sprague-Dawley rats inhaled 1.0 minimum alveolar concentration (MAC) sevoflurane, 1.5 MAC sevoflurane,or O(2) for 1 h. After 24 h and 48 h the left coronary artery of rats was occluded for 30 min,followed by 120 min of reperfusion. Hemodynamics was continuously recorded and myocardial infarct size was determined by Evans blue and triphenyltetrazolium chloride staining. The expression of nitric oxide synthase (NOS) was assessed by immunoblotting.
RESULTS1.0 MAC sevoflurane and 1.5 MAC sevoflurane improved cardiac pump function after reperfusion and reduced myocardial infarct size with the increased iNOS expression (P<0.05). However,the expression of eNOS and p-eNOS was not affected (P>0.05). A selective iNOS inhibitor 1400 W abolished the cardioprotection effect induced by inhalation of 1.0 MAC sevoflurane for 24 h.
CONCLUSIONSevoflurane produces delayed cardioprotection through the up-regulation of iNOS expression.
