Effects of acute angiotensin II on ischemia reperfusion injury following myocardial infarction. (March 2015)

• Record Type: Journal Article
• Authors: Mann, Sarah; Bajulaiye, Akinyemi; Sturgeon, Kathleen; Sabri, Abdelkarim; Muthukumaran, Geetha; Libonati, Joseph R.
• Is Part Of: Journal of the renin-angiotensin-aldosterone system. Volume 16:Number 1(2015:Mar.)
• Page Start: 13
• Page End: 22
• Publication Date: 2015-03
• Subjects: Left ventricle -- hormones -- preconditioning -- acidosis; Renin-angiotensin system -- Periodicals; 616.132
• DOI: 10.1177/1470320314554963
• Languages: English
• ISSNs: 1470-3203

Abstract

Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to subsequent ischemic events. While chronic angiotensin II blockade is cardioprotective post-MI, the acute effects of angiotensin II in ischemia-reperfusion injury (IR) remains unclear. In the present study, we tested whether angiotensin II administration altered recovery of left ventricular (LV) function to IR in hearts from sham and MI rats. Echocardiography, LV pressure-volume relationships, and IR performance were established in subsets of sham ( N = 27) and MI hearts ( N = 41). IR was conducted in red-cell-perfused Langendorff hearts (60 minutes of low-flow ischemia; 30 minutes of reperfusion) during vehicle or angiotensin II infusions (10 −7 M). MI hearts were dilated and had reduced fractional shortening and blunted systolic elastance ( p < 0.05). Despite systolic dysfunction in MI, functional recovery to IR was similar to sham. Angiotensin II significantly worsened IR performance in sham ( p < 0.05), but not MI. The effect of angiotensin II on in vitro cardiomyocyte survival under various pH conditions was also tested. Acidosis increased cardiomyocyte death and angiotensin II potentiated this effect. We conclude that IR performance is similar between sham and MI hearts and that MI hearts are resistant to angiotensin II-induced cardiac dysfunction in response to IR.