Exacerbation of left ventricular ischemic diastolic dysfunction by pressure-overload hypertrophy. Modification by specific inhibition of cardiac angiotensin converting enzyme.

摘要: Hearts with compensatory pressure-overload hypertrophy show an increased intracardiac activation of angiotensin II that may contribute to ischemic diastolic dysfunction. We studied whether in response aortic banding would result exaggerated dysfunction during low-flow ischemia and the specific inhibition cardiac converting enzyme by enalaprilat modify systolic function reperfusion either hypertrophied or nonhypertrophied hearts. Isolated, red blood cell-perfused isovolumic rat hearts were subjected (2.5 x 10(-7) M final concentration) infusion 20 minutes baseline perfusion 30 reperfusion. Coronary flow per gram was similar perfusion, ischemia, At baseline, left ventricular developed pressure higher than untreated groups (224 +/- 8 versus 150 9 mm Hg; p less 0.01) enalaprilat-treated (223 145 0.01). During depressed but all groups. All showed deterioration function; however, end-diastolic a significantly level (65 7 33 3 0.001). Enalaprilat had no effect hearts, it attenuated greater increase treated compared drug 50 5 The beneficial could not be explained differences coronary weight, glycolytic flux as reported lactate production, myocardial water content, oxygen consumption, tissue levels glycogen high energy phosphate compounds. reperfusion, partial recovery 70-74% initial values. No detected on restoration In conclusion, our experiments manifest severe impairment relaxation comparison control Further, support hypothesis enhanced conversion I rats contributes sensitivity ischemia.