Teoh K H, Mickle D A, Weisel R D, Fremes S E, Christakis G T, Romaschin A D, Harding R S, Madonik M M, Ivanov J
Division of Cardiovascular Surgery, Toronto General Hospital, Ontario, Canada.
J Surg Res. 1988 Jan;44(1):36-44. doi: 10.1016/0022-4804(88)90120-5.
Myocardial substrate preferences following cardioplegic arrest for coronary bypass surgery have not been established. Fatty acids are believed to be the major fuel source for aerobic metabolism. Following cardioplegic arrest arterial fatty acid levels are elevated and myocardial fatty acid accumulation without oxidation may contribute to reperfusion injury. Perioperative fatty acid metabolism was evaluated in 18 patients undergoing elective coronary bypass surgery who were randomized to receive either blood (n = 11) or crystalloid (n = 7) cardioplegia. Palmitate labeled with 14carbon was infused perioperatively and arterial and coronary sinus blood samples were obtained to calculate myocardial fatty acid extraction and oxidation before and after cardioplegic arrest. Lactate and glycerol were released from the heart during both blood and crystalloid cardioplegia, suggesting ischemic glycolysis and lipolysis. Myocardial oxygen consumption was depressed and the myocardial consumptions of lactate, glucose, and fatty acids were minimal during the first 60 min after aortic clamp removal in both groups despite high arterial concentrations. Fatty acid oxidation was minimal after blood cardioplegia and was not found after crystalloid cardioplegia. Fatty acids were extracted by the heart, but were not aerobically metabolized following cardioplegic arrest. Myocardial fatty acid accumulation without oxidation may have been deleterious. The inability of the heart to oxidize exogenous fatty acids may reflect altered myocardial exogenous substrate preferences during reperfusion following coronary bypass surgery.
冠状动脉搭桥手术心脏停搏后心肌底物偏好尚未明确。脂肪酸被认为是有氧代谢的主要燃料来源。心脏停搏后动脉脂肪酸水平升高，心肌脂肪酸蓄积而未氧化可能导致再灌注损伤。对18例行择期冠状动脉搭桥手术的患者进行围手术期脂肪酸代谢评估，这些患者被随机分为接受血液停搏液（n = 11）或晶体停搏液（n = 7）两组。围手术期输注14碳标记的棕榈酸，采集动脉血和冠状窦血样本，以计算心脏停搏前后心肌脂肪酸摄取和氧化情况。血液停搏液和晶体停搏液期间心脏均释放乳酸和甘油，提示存在缺血性糖酵解和脂解。两组在主动脉阻断解除后的最初60分钟内，尽管动脉浓度较高，但心肌氧耗均降低，心肌对乳酸、葡萄糖和脂肪酸的消耗均极少。血液停搏后脂肪酸氧化极少，晶体停搏后未发现脂肪酸氧化。心脏摄取脂肪酸，但心脏停搏后未进行有氧代谢。心肌脂肪酸蓄积而未氧化可能有害。心脏无法氧化外源性脂肪酸可能反映了冠状动脉搭桥手术后再灌注期间心肌对外源性底物偏好的改变。
