[Myocardial ischemic reperfusion injury affected by the isozymes of nitric oxide synthase and their gene expression: experimental study].

OBJECTIVE: To study nitric oxide (NO), isozymes of NO synthase (NOS) and their gene expression in the isolated working rat heart after ischemia-reperfusion injury. METHODS: We quantified the gene expression of the isozymes of NOS by reverse transcription-polymerase chain reaction (RT-PCR), analyzed the myocardial NOS, malondialdehyde (MDA) content, NO, creatine phosphokinase (CPK) in effluent samples from coronary sinus, and measured the heart function before and after ischemia reperfusion. We also studied the effects of dexamethasone(Dex) and bradykinin(BK) introduced into cardioplegia on myocardial ischemia reperfusion injury. RESULTS: Our study demonstrated that the expression of constitutive NOS(cNOS) mRNA was downregulated and of inducible NOS(iNOS) mRNA upregulated with NO, cNOS decrease and iNOS increase during ischemia reperfusion injury. In Dex-treated group, compared with the control group of ischemia reperfusion, the expression of iNOS mRNA was downregulated, NO and iNOS were reduced, the recovery of myocardial dysfunction was ameliorated and MDA, CPK reduced. In BK-treated group, the expression of NOS mRNA showed no significant change, NO and cNOS were increased. The recovery of myocardial dysfunction was ameliorated. MDA, CPK were also reduced. CONCLUSION: These results indicated that up- and down-regulation of expression of NOS isozymes could be one of the important mechanisms for myocardial ischemic reperfusion injury. Downregulating the expression of iNOS mRNA and activating cNOS could be helpful in myocardial protection.