Effects of Intracoronary Propofol on Functional Recovery of Stunned Myocardium and Coronary Endothelium in Dogs / 대한마취과학회지

ABSTRACT

BACKGROUND: Oxygen-derived free radicals are known to contribute to tissue injury during myocardial ischemia and reperfusion. Recent in vitro studies have shown that propofol has potent antioxidant properties. The present study was aimed to investigate the effects of propofol on recovery of mechanical and coronary endothelial function in a myocardial stunning model. METHODS: Thirty-five dogs were acutely instrumented under halothane anesthesia to measure aortic and left ventricular pressure, pulmonary and left anterior descending coronary artery (LAD) flow, and subendocardial segment length. After completion of the surgery, halothane was replaced by fentanyl- midazolam. Animals were then subjected to 15 min of LAD occlusion and 3 hrs of reperfusion under either intracoronary (i.c.) propofol (5 microgram/mL, n=11; 20 microgramg/mL LAD flow, n=12) or vehicle (saline, n=12) for 1 hr beginning 30 min before LAD occlusion. Percent segment shortening (%SS) and the slope of the preload recruitable stroke work (Mw), as an index of regional myocardial contractility, and peak lengthening rate (dL/dtmax) and percent post-systolic shortening (%PSS), as an index of regional diastolic function, were evaluated. Coronary endothelial function was assessed by examining LAD flow response to i.c. acetylcholine (ACh, 1 microgram over I min) and i.c. sodium nitroprusside (SNP, 20 microgram over I min). The myocardial content of malondialdehyde (MDA) from LAD area was measured to evaluate lipid peroxidation. RESULTS: Despite equally severe ischemic dysfunction during LAD occlusion, recovery of %SS was significantly improved during reperfusion by either dose of propofol compared to controls. However, Mw recovered to the baseline within 60 min of reperfusion in all three groups. In addition, propofol-treated dogs showed better recovery of both indices of regional diastolic function (dL/dtmax and %PSS) as compared to controls. Ischemia-reperfusion similarly attenuated the increases in the LAD flow by ACh in all the groups, whereas it had no significant effect on these increases in LAD flow by SNP. The increase in MDA induced by ischemia and reperfusion was significantly suppressed by either dose of propofol. CONCLUSIONS: The results indicate that propofol attenuates mechanical but not coronary endothelial dysfunction in postischemic, reperfused myocardium in an open-chest canine model. The protective action of propofol against mechanical dysfunction is probably due to its effect to reduce lipid peroxidation.