This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Leor, J. Articles by Battler, A. Search for Related Content PubMed PubMed Citation Articles by Leor, J. Articles by Battler, A. Social Bookmarking                         What's this?

Failure of Captopril to Attenuate Myocardial Damage, Neutrophil Accumulation, and Mortality Following Coronary Artery Occlusion and Reperfusion in Rat

Neufeld Cardiac Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Sheba Medical Center, Tel Hashomer, Israel

Nira Varda-Bloom

Neufeld Cardiac Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Sheba Medical Center, Tel Hashomer, Israel

David Hasdai

Neufeld Cardiac Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Sheba Medical Center, Tel Hashomer, Israel

Zehava Ovadia

Neufeld Cardiac Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Sheba Medical Center, Tel Hashomer, Israel

Alexander Battler

Neufeld Cardiac Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Sheba Medical Center, Tel Hashomer, Israel

Captopril, a sulfhydryl-containing angiotensin-converting enzyme inhibitor, has been suggested as possessing antiischemic and antiinflammatory properties. To test the hypothesis that captopril may prevent neutrophil-induced myocardial injury during acute myocardial infarction (AMI), the authors subjected rats to coronary occlusion for thirty minutes and reperfusion for twenty-four hours (MI) or to sham operation (sham MI). Oral captopril (100 mg/kg) or vehicle was administered thirty minutes before coronary occlusion. The effect of captopril on mean arterial blood pressure was assessed in separate group of animals (n=8).

Infarct size and neutrophil accumulation in myocardium were determined by measuring creatine phosphokinase depletion and myeloperoxidase (MPO) activity, respectively, in the left ventricular free wall (LVFW). Animals treated with 100 mg/kg of captopril exhibited significant reduction in mean arterial blood pressure compared with vehicle-treated animals (P < 0.01). Compared with vehicle-treated animals, administra tion of 100 mg/kg of captopril to MI animals attenuated neither twenty-four-hour (continued on next page) mortality (56% vs 52%, respectively), nor infarct size (36 ± 7% vs 34% ± 7% respec tively), nor MPO activity (1.0 ±0.17 vs 1.26 ±0.19).

Thus, in the present experiment captopril did not reduce neutrophil-induced myocar dial damage following coronary occlusion and reperfusion. These findings may be partly explained by the negative effect of captopril on arterial blood pressure during AMI.

Angiology, Vol. 45, No. 8, 717-724 (1994)
DOI: 10.1177/000331979404500807


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?