Myocardial depression after elective ischemic arrest. Subcellular biochemistry and prevention.
The hemodynamic and cardiac biochemical effects of global ischemic arrest during cardiopulmonary bypass (CPB) were studied in 54 animals and compared to seven animals without ischemic arrest. Ischemic arrest alone reduced the first derivative of left ventricular force of contraction (LV dF/dt) to 52 percent of control 10 minutes after resuming function and to 64 percent after 1 hour of reperfusion. Cardiac output was depressed to 52 percent of control after 10 minutes of reperfusion, and to 74 percent of control after 60 minutes of reperfusion. In six animals, moderate hypothermia (26 degrees C.) resulted in no protection of cardiac function from ischemic arrest, whereas profound hypothermia to 18 degrees C. resulted in values of LV dF/dt and cardiac output nearly equivalent to the CPB control group (no arrest). A continuous infusion of a hyperkalemic hypothermic solution slightly improved the degree of protection over hypothermia alone. The sarcoplasmic reticulum (SR) isolated from hearts which had undergone 60 minutes of ischemic arrest bound significantly less calcium when the isolation was done after 10 minutes of reperfusion as well as when it was done after 60 minutes of reperfusion. The time to spontaneous release of calcium from the SR also was significantly longer. Moderate hypothermia did not result in improved SR function, whereas deep hypothermia induced by local cooling or by hypothermic potassium infusion retained SR function at normal levels. Oxidative phosphorylation of mitochondria isolated after 60 minutes of reperfusion was also depressed. The mitochondrial respiration rate after normothermic ischemic arrest was 155 natoms of oxygen per minutes versus 237 natoms for the hypothermic hyperkalemic group. Respiratory control index was 5.5 for the normothermic group versus 9.4 for the hypothermic group. It is concluded that hypothermia, whether effected by surface cooling or by hypothermic potassium infusion, allowed full recovery of hemodynamic and biochemical functions within 1 hour of reperfusion.
D000818:Animals; D002118:Calcium / Q000502:physiology; D002302:Cardiac Output; D002315:Cardiopulmonary Bypass; D003331:Coronary Vessels; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D007036:Hypothermia, Induced; D007511:Ischemia / Q000503:physiopathology*; D008929:Mitochondria, Heart / Q000503:physiopathology; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption; D011188:Potassium / Q000008:administration & dosage; D012519:Sarcoplasmic Reticulum / Q000503:physiopathology
D011188:Potassium; D002118:Calcium