Myocardial infarction and nitric oxide.
The report deals with the induction of the inducible form of nitric oxide synthase (iNOS) in infarcted heart muscle of rabbit and man. In the rabbit, nitric oxide synthase was significantly increased in the infarcted area beginning on the third day following ligation of a coronary artery. iNOS induction occurred primarily in macrophages. In man, iNOS immunoreactivity was also primarily localized in macrophages on the seventh day following death from myocardial infarction. Of the specific inhibitors of iNOS in infarcted heart muscle, S-methylisothiourea (SMT) was the most potent. Its greatest effect occurred in the normal non-affected area of the heart. Dexamethasone and cyclosporin A failed to inhibit iNOS. Apoptosis of macrophages commenced two days following ligation of a coronary artery.
Bing
R J
RJ
Department of Experimental Cardiology, Huntington Medical Research Institutes, Pasadena, CA 91101, USA.
Suzuki
H
H
D000818:Animals; D017209:Apoptosis; D016572:Cyclosporine / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004790:Enzyme Induction; D006801:Humans; D007550:Isothiuronium / Q000031:analogs & derivatives / Q000494:pharmacology; D009203:Myocardial Infarction / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism; D011817:Rabbits
D007550:Isothiuronium; D009569:Nitric Oxide; D003907:Dexamethasone; D016572:Cyclosporine; D019001:Nitric Oxide Synthase; C027744:S-methylisothiopseudouronium