• Lei-lei Ma, Feng-jiang Zhang, and Min Yan.
• Department of Anesthesiology, Zhejiang University School of Medicine, Hangzhou, China.
• Zhejiang Da Xue Xue Bao Yi Xue Ban. 2012 Sep 1;41(5):553-8.

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.

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