Abstract: Objective To observe the role of iNOS in cardiomyocyte apoptosis of rat trauma model. Methods Trauma rats model was established by Noble-Collip drum. Cardiomyocyte apoptosis was determined by Caspase-3 activity and DNA ladder detection. The protein expression if iNOS was investigated by Western blot. Nitric oxide (NO) content in myocardial tissue was detected by chemiluminescene method. Myocardial nitrotyrosine (NT) content was measured by ELISA. Results Cardiomyocyte apoptosis was increased in mechanical trauma (P<0.01). Myocardial iNOS expression obviously increased after trauma (P<0.01). In addition, the product of NO2-/NO3- and NT, was elevated significantly in myocardial tissue after trauma (P<0.01). 1400W, a selective inhibition of iNOS, significantly decreased cardiomyocyte apoptosis(P<0.05), and the product of NO2-/NO3- and NT (NO2-/NO3-: P<0.01; NT: P<0.05). Conclusion iNOS caused cardiomyocyte apoptosis by increasing the levels of NO and peroxynitrite acid in myocardial tissue.

Key words: heart injuries, nitric oxide synthase, nitric oxide, peroxynitrite acid, apoptosis