Effects of pulsatile reperfusion on postischemic recovery of myocardial function after global hypothermic cardiac arrest.
It has been postulated that pulsatile blood flow helps to preserve the myocardium after ischemia. However, its effect on postischemic myocardium during cardiopulmonary bypass has not been clearly defined. To determine if pulsatile reperfusion improves postischemic recovery of cardiac metabolism and performance, we subjected 20 dogs to 60 minutes of aortic cross-clamping followed by 45 minutes of pulsatile (P group; 10 dogs) or nonpulsatile (NP group; 10 dogs) reperfusion. Left ventricular function was measured at a controlled preload in both groups before induction of global ischemia and after termination of bypass. Segmental length (assessed by sonomicrometry) was used to determine dimensional changes. Ventricular pressures were measured with solid-state micromanometers. Percent recovery of left ventricular peak systolic pressure, its first derivative, and stroke work were 66%, 59%, and 38%, respectively in the NP group and 82%, 76%, and 65% in the P group. The postarrest decrease in segmental shortening was minimized in the P group; left ventricular function curves and the slope of the end-systolic pressure-length relationship also indicated better performance after pulsatile reperfusion than after nonpulsatile reperfusion. Myocardial lactate extraction was transiently improved during the early pulsatile reperfusion period. We conclude that pulsatile reperfusion provides better myocardial preservation than nonpulsatile perfusion after 60 minutes of induced global ischemia.
D000818:Animals; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D007036:Hypothermia, Induced; D007773:Lactates / Q000097:blood / Q000378:metabolism; D019344:Lactic Acid; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion / Q000379:methods; D011673:Pulsatile Flow; D012212:Rheology
D007773:Lactates; D019344:Lactic Acid