Low-dose inotropic stimulation during left ventricular ischaemia does not worsen post-ischaemic dysfunction

Objective: Inotropic agents are used clinically to improve ventricular function during ischaemia. The goal of this study was to determine whether inotropic stimulation during moderate left ventricular (LV) ischaemia exacerbates post-ischaemic LV dysfunction. Methods: In 18 open-chest, anesthetized pigs, LV pressure versus subendocardial segment length loops were used to generate regional preload-recruitable stroke work (PRSW) and LV end-diastolic pressure (EDP) versus end-diastolic segment length (EDL) relations. Ischaemia was produced by constant, partial constriction of the mid anterior descending coronary artery for 90 min. Nine pigs received dobutamine (4 mu g . kg(-1). min(-1), i.v.) during the final 60 min of ischaemia (Group 2), while 9 other pigs did not (Group 1). Results: During unstimulated ischaemia, anterior subendocardial blood flow (Group 1, 0.27+/-.05; Group 2, 0.30+/-.07 ml . g(-1). min(-1), mean+/-s.e.m.) and steady-state PRSW (Group 1, 30+/-4%; Group 2, 27+/-5% of baseline) were similar in both groups. Dobutamine stimulation during ischaemia increased heart rate, mean arterial pressure, subendocardial blood flow, oxygen consumption and steady-state PRSW of the ischaemic zone, but not lactate release. After 60 min reperfusion, steady-state ischaemic zone PRSW remained markedly and nearly equally reduced in both groups (Group 1, 28+/-4%; Group 2, 23+/-5% of baseline). Reduced PRSW after reperfusion was due primarily to persistent rightward shift of the PRSW intercept with only a modest contribution from reduced PRSW slope. Conclusions: Low-dose inotropic stimulation during moderate regional LV ischaemia increases aerobic, but not anaerobic energy metabolism, and does not worsen post-ischaemic dysfunction.