TY - JOUR
T1 - Failure of Captopril to Attenuate Myocardial Damage, Neutrophil Accumulation, and Mortality Following Coronary Artery Occlusion and Reperfusion in Rat
AU - Leor, Jonathan
AU - Varda-Bloom, Nira
AU - Hasdai, David
AU - Ovadia, Zehava
AU - Battler, Alexander
PY - 1994/8
Y1 - 1994/8
N2 - 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 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.
AB - 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 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.
UR - http://www.scopus.com/inward/record.url?scp=0028029420&partnerID=8YFLogxK
U2 - 10.1177/000331979404500807
DO - 10.1177/000331979404500807
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AN - SCOPUS:0028029420
SN - 0003-3197
VL - 45
SP - 717
EP - 724
JO - Angiology
JF - Angiology
IS - 8
ER -