Görge G, Papageorgiou I, Lerch R
Cardiology Center, University Hospital, Geneva, Switzerland.
Basic Res Cardiol. 1990 Nov-Dec;85(6):595-605. doi: 10.1007/BF01907894.
Recovery of contractile function and of fatty acid oxidation may be delayed in viable postischemic myocardium. To determine whether a metabolic reserve is preserved after reperfusion of reversibly injured myocardium, we studied the effect of epinephrine on myocardial fatty acid oxidation in isolated rat hearts perfused retrogradely with erythrocyte enriched buffer containing albumin 0.4 mM, palmitate 0.4 mM, and glucose 11 mM. Hearts were subjected to 60 min of low-flow ischemia (5% of control flow) followed by 60 min of reperfusion. Five minutes following the onset of reperfusion, developed left ventricular pressure (DLVP) and oxidation of palmitate were reduced to 53% (p less than 0.01) and 46% (p less than 0.01), respectively, of values measured in nonischemic control hearts. Subsequently, DLVP and oxidation of palmitate gradually recovered to 78% (NS) and 91% (NS) by 60 min of reperfusion. Epinephrine 5.10(-1) M elicited an immediate stimulation of both contractile function and palmitate oxidation. Early after reperfusion stimulated DLVP and palmitate oxidation were still lower compared to values measured in control hearts exposed to the same concentration of epinephrine. Later than 15 min after the onset of reperfusion the response of DLVP and of palmitate oxidation to epinephrine no longer differed between control and reperfused hearts. These results indicate that viable postischemic myocardium exhibits a remarkable oxidative metabolic reserve. The observation provides further evidence for the view that impairment of myocardial energy production is not responsible for contractile dysfunction early after reperfusion.
在存活的缺血后心肌中，收缩功能和脂肪酸氧化的恢复可能会延迟。为了确定可逆性损伤心肌再灌注后代谢储备是否得以保留，我们研究了肾上腺素对离体大鼠心脏心肌脂肪酸氧化的影响，这些心脏用含有0.4 mM白蛋白、0.4 mM棕榈酸盐和11 mM葡萄糖的富红细胞缓冲液进行逆行灌注。心脏先经历60分钟的低流量缺血（对照流量的5%），然后再灌注60分钟。再灌注开始后5分钟，左心室舒张末压（DLVP）和棕榈酸盐氧化分别降至非缺血对照心脏测量值的53%（p<0.01）和46%（p<0.01）。随后，到再灌注60分钟时，DLVP和棕榈酸盐氧化逐渐恢复到78%（无统计学意义）和91%（无统计学意义）。5×10⁻¹M肾上腺素立即刺激了收缩功能和棕榈酸盐氧化。再灌注早期，与暴露于相同浓度肾上腺素的对照心脏相比，刺激后的DLVP和棕榈酸盐氧化仍然较低。再灌注开始15分钟后，对照心脏和再灌注心脏中DLVP和棕榈酸盐氧化对肾上腺素的反应不再有差异。这些结果表明，存活的缺血后心肌表现出显著的氧化代谢储备。这一观察结果为以下观点提供了进一步的证据，即心肌能量产生受损并非再灌注后早期收缩功能障碍的原因。
