Schwaiger M, Schelbert H R, Keen R, Vinten-Johansen J, Hansen H, Selin C, Barrio J, Huang S C, Phelps M E
J Am Coll Cardiol. 1985 Aug;6(2):311-20. doi: 10.1016/s0735-1097(85)80166-2.
Free fatty acids are the major energy source for cardiac muscle. Oxidation of fatty acid decreases or even ceases during ischemia. Its recovery after transient ischemia remains largely unexplored. Using intracoronary carbon-11 palmitic acid as a tracer of myocardial fatty acid metabolism in an open chest dog model, retention and clearance of tracer in myocardium were evaluated at control, during ischemia and after reperfusion following a 20 minute occlusion of the left anterior descending coronary artery. Myocardial C-11 time-activity curves were analyzed with biexponential curve-fitting routines yielding fractional distribution and clearance half-times of C-11 palmitic acid in myocardial tissue. In animals with permanent occlusion and intracoronary injection of C-11 palmitic acid distal to the occlusion site, the relative size and half-time of the early clearance curve component differed markedly from control values and did not change with ongoing ischemia. Conversely, in animals with only 20 minutes of coronary occlusion, the relative size of the early C-11 clearance phase was still significantly depressed at 20 and 90 minutes of reperfusion but returned to control level at 180 minutes. Tissue C-11 clearance half-times remained significantly prolonged throughout the reperfusion period. Regional function in reperfused myocardium monitored with ultrasonic crystals recovered slowly and was still less than control after 3 hours of reperfusion. The data indicate that after transient ischemia, myocardial fatty acid metabolism fails to recover immediately. Because the metabolic recovery occurs in parallel with recovery of regional function, C-11 palmitic acid in conjunction with positron tomography may be useful for studying regional fatty acid metabolism noninvasively after an ischemic injury, and may be helpful in identifying reversible tissue injury.
游离脂肪酸是心肌的主要能量来源。在缺血期间，脂肪酸氧化减少甚至停止。短暂缺血后其恢复情况在很大程度上仍未得到探索。在开胸犬模型中，使用冠状动脉内碳 - 11棕榈酸作为心肌脂肪酸代谢的示踪剂，在左前降支冠状动脉闭塞20分钟后的对照期、缺血期和再灌注期评估示踪剂在心肌中的滞留和清除情况。用双指数曲线拟合程序分析心肌碳 - 11时间 - 活性曲线，得出碳 - 11棕榈酸在心肌组织中的分布分数和清除半衰期。在永久性闭塞并在闭塞部位远端冠状动脉内注射碳 - 11棕榈酸的动物中，早期清除曲线成分的相对大小和半衰期与对照值明显不同，并且不随持续缺血而改变。相反，在仅冠状动脉闭塞20分钟的动物中，再灌注20分钟和90分钟时早期碳 - 11清除阶段的相对大小仍显著降低，但在180分钟时恢复到对照水平。在整个再灌注期间，组织碳 - 11清除半衰期仍显著延长。用超声晶体监测的再灌注心肌区域功能恢复缓慢，再灌注3小时后仍低于对照水平。数据表明，短暂缺血后，心肌脂肪酸代谢不能立即恢复。由于代谢恢复与区域功能恢复同时发生，碳 - 11棕榈酸结合正电子断层扫描可能有助于无创研究缺血性损伤后区域脂肪酸代谢，并有助于识别可逆性组织损伤。
