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DO ANGIOTENSIN CONVERTING ENZYME INHIBITORS LIMIT MYOCARDIAL INFARCT SIZE?
Author(s) -
Miki Takayuki,
Miura Tetsuji,
Shimamoto Kazuaki,
Urabe Kazuyuki,
Sakamoto Jun,
Iimura Osamu
Publication year - 1993
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1993.tb01720.x
Subject(s) - myocardial infarction , angiotensin converting enzyme , cardiology , enzyme , medicine , limit (mathematics) , chemistry , pharmacology , biochemistry , blood pressure , mathematics , mathematical analysis
SUMMARY 1. Effects of captopril, ramiprilat and Hoe 140, a specific bradykinin receptor antagonist, on infarct size were assessed in a rabbit model of myocardial infarction. 2. Rabbits were untreated or pretreated with 0.5 mg/kg of captopril, 0.05 mg/kg of ramiprilat or 20 nmol/kg of Hoe 140 before 30 min coronary artery occlusion and 72 h reperfusion. 3. Captopril and ramiprilat treatment reduced systemic blood pressure by about 10 mmHg without alteration of heart rate, and the dose of Hoe 140 almost completely blocked hypotensive response to intravenous injection of bradykinin (100 ng/kg). 4. Infarct size expressed as percentage of area at risk was 44.5 ± 3.3% in the control group, 41.9 ± 1.6% in the captopril group, 51.8 ± 2.7% in the ramiprilat group and 46.7 ± 2.2% in the Hoe 140 group. All percentages were not significantly different. 5. These data suggest that angiotensin converting enzymes (ACE), with or without sulfhydryl groups do not limit myocardial infarct size and that endogenous bradykinin in ischaemic myocardium does not play a major protective role against ischaemic myocardial necrosis.