Chatelain P, Papageorgiou I, Luthy P, Melchior J P, Rutishauser W, Lerch R
Cardiology Center, University Hospital, Geneva, Switzerland.
Basic Res Cardiol. 1987;82 Suppl 1:169-76. doi: 10.1007/978-3-662-08390-1_21.
To assess whether myocardial lipid metabolism is altered in the "stunned" myocardium we have studied the metabolism of (1-14C)-palmitate during reperfusion in a modified rat heart preparation. Hearts were perfused retrogradely at a physiological flow rate (2 ml/min) in a non-recirculating system with erythrocyte-enhanced Krebs-Henseleit buffer containing albumin 0.4 mM, glucose 11 mM, palmitate 0.4 mM and trace amounts of (1-14C)-palmitate. Left ventricular pressure was measured by a latex balloon in the left ventricular cavity. Control hearts were perfused at constant flow for 120 min. To achieve reversible ischaemic damage, myocardial perfusion was reduced by 95% for 40 min, followed by reperfusion at the control flow rate for 60 min (reperfusion group). For comparison, irreversible damage was produced by calcium free perfusion (calcium paradox group). In the reperfusion group, the developed pressure was severely depressed 5 min after reperfusion to 23% of the value in the control group (p less than 0.05) but recovered to 84% (NS) at 60 min. In the calcium paradox group, mechanical activity ceased completely without recovery. Myocardial uptake of (1-14C)-palmitate in the reperfusion group was similar to the control experiments for the entire reperfusion period, whereas a marked depression was observed in the calcium paradox group. 14CO2 production was severely depressed at the onset of reperfusion in both the reperfusion and calcium paradox group to 42% (p less than 0.05) and 29% (p less than 0.05) respectively. In contrast to the calcium paradox group, 14CO2 production in the reperfusion group recovered progressively to 70% (NS) of the control value during the 60 min of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
为了评估“顿抑”心肌中心肌脂质代谢是否改变，我们在改良的大鼠心脏标本中研究了再灌注期间（1-14C）-棕榈酸酯的代谢。心脏在非循环系统中以生理流速（2毫升/分钟）逆行灌注，所用缓冲液为红细胞强化的克雷布斯-亨塞尔特缓冲液，其中含有0.4毫摩尔/升白蛋白、11毫摩尔/升葡萄糖、0.4毫摩尔/升棕榈酸酯和微量的（1-14C）-棕榈酸酯。通过左心室腔中的乳胶气球测量左心室压力。对照心脏以恒定流速灌注120分钟。为造成可逆性缺血损伤，将心肌灌注减少95%，持续40分钟，然后以对照流速再灌注60分钟（再灌注组）。为作比较，通过无钙灌注造成不可逆损伤（钙反常组）。在再灌注组中，再灌注5分钟后，左心室舒张末压严重降低至对照组值的23%（p<0.05），但在60分钟时恢复至84%（无显著性差异）。在钙反常组中，机械活动完全停止且未恢复。再灌注组中（1-14C）-棕榈酸酯的心肌摄取在整个再灌注期间与对照实验相似，而在钙反常组中观察到显著降低。在再灌注组和钙反常组中，再灌注开始时14CO2生成均严重降低，分别降至42%（p<0.05）和29%（p<0.05）。与钙反常组不同，再灌注组中的14CO2生成在60分钟的再灌注期间逐渐恢复至对照值的70%（无显著性差异）。（摘要截短于250词）
