{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,6,27]],"date-time":"2025-06-27T19:45:45Z","timestamp":1751053545165},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[1998,6]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Angiotensin-converting enzyme (ACE) inhibitors increase the production of nitric oxide (NO) and prostacyclin and open Ca\n            <jats:sup>2+<\/jats:sup>\n            -activated K\n            <jats:sup>+<\/jats:sup>\n            channels. The effects of these actions of ACE inhibitors on infarct size were investigated in open-chest dogs subjected to myocardial ischemia and reperfusion. Infarct size was assessed 6 hours after the onset of reperfusion, subsequent to 90 minutes of occlusion of the left anterior descending coronary artery. The ACE inhibitor cilazaprilat was administered into the coronary artery 10 minutes before coronary occlusion, and infusion was continued until 1 hour after reperfusion. The bradykinin and NO concentrations in coronary venous blood 10 minutes after the onset of reperfusion were significantly higher in dogs treated with cilazaprilat (3 \u03bcg \u00b7 kg\n            <jats:sup>-1<\/jats:sup>\n            \u00b7 min\n            <jats:sup>-1<\/jats:sup>\n            ) than in control animals. Although there were no significant differences in collateral flow during ischemia, infarct size in the cilazaprilat group was smaller than that in the control group (15.1\u00b13.0% versus 46.7\u00b14.2% of the area at risk,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.0001). The infarct size\u2013limiting effect of cilazaprilat was partially reduced by either\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>G<\/jats:sup>\n            -nitro-\n            <jats:sc>l<\/jats:sc>\n            -arginine methyl ester (an inhibitor of NO synthase) or iberiotoxin (a blocker of Ca\n            <jats:sup>2+<\/jats:sup>\n            -activated K\n            <jats:sup>+<\/jats:sup>\n            channels) and was abolished by\n            <jats:italic>N<\/jats:italic>\n            <jats:sup>G<\/jats:sup>\n            -nitro-\n            <jats:sc>l<\/jats:sc>\n            -arginine methyl ester plus iberiotoxin. Indomethacin (an inhibitor of cyclooxygenase) had no effect on the beneficial action of cilazaprilat. Inhibition of ACE thus reduced myocardial infarct size, an effect that was mediated by NO and the opening of Ca\n            <jats:sup>2+<\/jats:sup>\n            -activated K\n            <jats:sup>+<\/jats:sup>\n            channels in canine hearts.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.31.6.1290","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:53:46Z","timestamp":1339462426000},"page":"1290-1298","update-policy":"http:\/\/dx.doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":23,"title":["Role of Ca\n            <sup>2+<\/sup>\n            -Activated K\n            <sup>+<\/sup>\n            Channels in the Protective Effect of ACE Inhibition Against Ischemic Myocardial Injury"],"prefix":"10.1161","volume":"31","author":[{"given":"Koichi","family":"Node","sequence":"first","affiliation":[{"name":"From the First Departments of Medicine (K.N., M.K., T.M., M.H.) and of Physiology (H.K.), Osaka University School of Medicine, and the Department of Physiology, Tokai University, Isehara (H.M.), Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masafumi","family":"Kitakaze","sequence":"additional","affiliation":[{"name":"From the First Departments of Medicine (K.N., M.K., T.M., M.H.) and of Physiology (H.K.), Osaka University School of Medicine, and the Department of Physiology, Tokai University, Isehara (H.M.), Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiroaki","family":"Kosaka","sequence":"additional","affiliation":[{"name":"From the First Departments of Medicine (K.N., M.K., T.M., M.H.) and of Physiology (H.K.), Osaka University School of Medicine, and the Department of Physiology, Tokai University, Isehara (H.M.), Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Tetsuo","family":"Minamino","sequence":"additional","affiliation":[{"name":"From the First Departments of Medicine (K.N., M.K., T.M., M.H.) and of Physiology (H.K.), Osaka University School of Medicine, and the Department of Physiology, Tokai University, Isehara (H.M.), Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hidezo","family":"Mori","sequence":"additional","affiliation":[{"name":"From the First Departments of Medicine (K.N., M.K., T.M., M.H.) and of Physiology (H.K.), Osaka University School of Medicine, and the Department of Physiology, Tokai University, Isehara (H.M.), Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Masatsugu","family":"Hori","sequence":"additional","affiliation":[{"name":"From the First Departments of Medicine (K.N., M.K., T.M., M.H.) and of Physiology (H.K.), Osaka University School of Medicine, and the Department of Physiology, Tokai University, Isehara (H.M.), Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.16.4.363"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.18.4.558"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0022-2828(92)91103-C"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1995.1823"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.92.4.1005"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.93.2.356"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.70.3.1537096"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.72.2.8418991"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.27.1.7"},{"key":"e_1_3_2_10_2","first-page":"H830","volume":"261","year":"1991","unstructured":"Cowan CL, Cohen RA. 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