Stunned myocardium may be mediated by intracellular Ca2+ overloading or oxygen derived-free radicals. Halothane and propofol have been shown to block Ca2+ channels. Propofol is also known to have antioxidant properties. The present study was aimed to investigate the effects of anesthetics on recovery of postischemic, reperfused myocardium in open-chest dogs. Incidence of ventricular arrhythmia upon ischemia and reperfusion was also determined.

Forty dogs were subjected to 15 min occlusion of left anterior descending coronary artery (LAD) followed by 3 hr reperfusion during halothane (n=10), fentanyl (n=12), or propofol plus fentanyl (n=11) anesthesia. Regional contractile function was assessed using percent systolic shortening (%SS), the preload recruitable stroke work slope (Mw), and peak systolic intramyocardial pressure (IMPs). Diastolic function was evaluated using time constant for isovolumic intramyocardial pressure decline of left ventricle (IMP-tau) and percent post-systolic shortening (%PSS).

%SS in the halothane, fentanyl, and propofol-fentanyl groups was similar at 3 hours of reperfusion (58%, 60%, and 55% of baseline value, respectively). Moreover, Mw recovered to the baseline values in the early reperfusion period in all three groups. However, IMP-tau was significantly prolonged in the halothane group throughout the 3 hour reperfusion period, whereas it remained unchanged in the fentanyl and propofol-fentanyl groups. Coronary occlusion was associated with 9, 33, and 0% mortality rate due to ventricular fibrillation upon ischemia and reperfusion in the halothane, fentanyl, and propofol-fentanyl groups, respectively.

These findings indicate that halothane, but not fentanyl and propofol- fentanyl, impairs myocardial relaxation, while recovery pattern of contractile function do not differ among three groups, and that halothane and propofol reduce reperfusion arrhythmia in the canine model of myocardial stunning.