Participation of Nitric Oxide and Peroxynitrite in the Development of Myocardial Tissue Damage in Acute Myocardial Infarction

• Published in: Cardiovascular pathology 1998-01, Vol.7 (1), p.25-30
• Main Authors: Shimojo, Takashi, Nishikawa, Toshio, Ishiyama, Shigeru, Ikeda, Ikuo, Kasajima, Takeshi, Marumo, Fumiaki, Hiroe, Michiaki
• Format: Article
• Language: English
• ISSN: 1054-8807; 1879-1336
• DOI: 10.1016/S1054-8807(97)00021-5

Many factors, including superoxides, contribute to tissue damage in acute myocardial infarction (AMI). Excess nitric oxide (NO) produced by inducible NO synthase (iNOS) has also been reported to participate in myocardial injury associated with AMI, but its exact role remains unclear. To elucidate the role of NO and peroxynitrite in the pathogenesis of myocardial injury associated with AMI, we examined the expression of iNOS in the autopsied specimens of the left ventricle obtained from 15 patients with AMI and five with old MI by immunohistochemistry using an anti-iNOS polyclonal antibody. The distribution of nitrotyrosine was also examined immunohistochemically. In patients who died from 12 hours to 3 weeks after the infarction, positive immunoreactivity for iNOS was observed in residual myocytes, macrophages, and vascular endothelial cells in the peri-infarcted area. Degenerating myocytes in that area in all of that group showing positive staining for iNOS were also stained positive for anti-nitrotyrosine antibody selfsame. These findings were not observed in the myocardial specimens obtained from patients who died within 12 hours after the onset of AMI, showing a minimal number of inflammatory cells, or in the specimens from patients with an old myocardial infarction, which showed scar tissue and no cellular infiltration. Inducible NOS and nitrotyrosine were expressed in damaged myocardium from patients with AMI, suggesting that the NO radical and peroxynitrite are involved in the pathogenesis of myocardial damage.