title: Protective effect of captopril on ischemic myocardium.
abstract: The protective effect and mechanism of action of the angiotensin-converting enzyme inhibitor (ACE-I) captopril was investigated in organelles from ischemic myocardial cells in a canine coronary ligation model. Sarcoplasmic reticulum (SR) and mitochondrial fractions were extracted from ischemic and nonischemic myocardial cells from captopril- and saline-treated (control) hearts. Heart rate, cardiac output, and right ventricular systolic blood pressure were similar in the captopril-treated and control groups. Left ventricular systolic blood pressure (LVPs) decreased gradually to 89% of the baseline value after captopril administration, and to 78% of the baseline value after ligation. Ca-ATPase activity in the SR, the respiratory control ratio (RCR) in the mitochondria, and dinitrophenol (DNP)-stimulated ATPase activity were significantly higher in ischemic myocardium from the captopril-treated group than from the saline-treated (control) group. The SH group content of both organelles was higher in the captopril-treated group. Our results suggest that, in addition to their hemodynamic effects, ACE-I agents containing SH groups protect the myocardium from ischemic damage by preventing enzyme oxidation.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Yanagishita
authors.forename: M
authors.initials: M
authors.lastname: Tomita
authors.forename: S
authors.initials: S
authors.lastname: Itoh
authors.forename: S
authors.initials: S
authors.lastname: Mukae
authors.forename: H
authors.initials: H
authors.lastname: Arata
authors.forename: H
authors.initials: H
authors.lastname: Ishioka
authors.forename: E
authors.initials: E
authors.lastname: Geshi
authors.forename: N
authors.initials: N
authors.lastname: Konno
authors.forename: T
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000818:Animals; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002216:Captopril / Q000627:therapeutic use*; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D008565:Membrane Proteins / Q000378:metabolism; D008929:Mitochondria, Heart / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D012519:Sarcoplasmic Reticulum / Q000201:enzymology / Q000378:metabolism; D013438:Sulfhydryl Compounds / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D008565:Membrane Proteins; D013438:Sulfhydryl Compounds; D002216:Captopril; D016660:NAD(P)H Dehydrogenase (Quinone); D000252:Calcium-Transporting ATPases