Effects of amrinone on experimental acute myocardial ischaemic injury

Publisher Website
Google Scholar
Abstract
This study was performed to assess the effects of the promising new inotropic agent amrinone on acute myocardial ischaemic injury in the anaesthetised, non-failing canine heart. Eight dogs underwent serial 15 min coronary artery occlusion (CAO) with intervening periods of coronary reperfusion. Saline was infused during the control CAO and amrinone or isoprenaline was infused intravenously at rates necessary to raise left ventricular dP/dt (LV dP/dt) by equivalent amounts in the latter two CAOs. Summed epicardial ST segment elevation (ΣST) was 42.9 ± 14.9 mV in the control CAO, but increased significantly to 76.1 ± 14.4 mV during CAO with amrinone infusion and to 68.6 ± 16.4 mV during CAO with isoprenaline infusion (PPco2 (Pm,co2) during a control CAO (saline infusion) and CAO with amrinone or isoprenaline infused to raise LV dP/dt by equivalent amounts in seven dogs. The magnitude of Pm,co2 rise from baseline(ΔPm,co2) was 6.0 ± 0.5 kPa (45.3 ± 3.9 mmHg) for the control CAO, and was significantly higher during CAO with amrinone or isoprenaline infusion (8.7 ± 0.7 and 8.5 ± 1.0 kPa (64.9 ± 5.0 and 63.7 ± 7.2 mmHg), P Pm,co2 in consecutive CAO's without inotropic stimulation were documented in further studies. We conclude that amrinone, when infused to produce positive inotropic effects equivalent to those of isoprenaline, is equally detrimental in increasing acute myocardial ischaemic injury in the non-failing canine heart, as manifest by augmentation of epicardial ST segment elevation and intramyocardial Pco2 with both agents during coronary occlusion.