Stoner Jason D, Angelos Mark G, Clanton Thomas L
Dept. of Emergency Medicine, Ohio State Univ., 146 Means Hall, 1654 Upham Dr., Columbus, OH 43210, USA.
Am J Physiol Heart Circ Physiol. 2004 Jan;286(1):H375-80. doi: 10.1152/ajpheart.00436.2003. Epub 2003 Sep 4.
The degree of myocardial oxygen delivery (Do2) that is necessary to reestablish functional contractile activity after short-term global ischemia in heart is not known. To determine the relationship between Do2 and recovery of contractile and metabolic functions, we used tissue NADH fluorometric changes to characterize adequacy of reperfusion flow. Isolated perfused rat hearts were subjected to global ischemia and were reperfused at variable flow rates that ranged from 1 to 100% of baseline flow. Myocardial function and tissue NADH changes were continuously measured. NADH fluorescence rapidly increased and plateaued during ischemia. A strong inverse logarithmic correlation between NADH fluorescence and reperfusion Do2 was demonstrated (r = -0.952). Left ventricular function (rate-pressure product) was inversely related to NADH fluorescence at reperfusion flows from 25 to 100% of baseline (r = -0.922) but not at lower reperfusion flow levels. An apparent reperfusion threshold of 25% of baseline Do2 was necessary to resume contractile function. At very low reperfusion flows (1% of baseline), another threshold flow was identified at which NADH levels increased beyond that observed during global ischemia (3.4 +/- 3.0%, means +/- SE, n = 9), which suggests further reduction of the cellular redox state. This NADH increase at 1% of baseline reperfusion flow was blocked by removing glucose from the perfusate. NADH fluorescence is a sensitive indicator of myocardial cellular oxygen utilization over a wide range of reperfusion Do2 values. Although oxygen is utilized at very low flow rates, as indicated by changes in NADH, a critical threshold of approximately 25% of baseline Do2 is necessary to restore contractile function after short-term global ischemia.
心脏短期整体缺血后恢复功能性收缩活动所需的心肌氧输送（Do2）程度尚不清楚。为了确定Do2与收缩和代谢功能恢复之间的关系，我们使用组织NADH荧光变化来表征再灌注血流的充足性。将离体灌注的大鼠心脏进行整体缺血，并以基线血流的1%至100%的不同流速进行再灌注。连续测量心肌功能和组织NADH变化。NADH荧光在缺血期间迅速增加并达到平台期。结果表明NADH荧光与再灌注Do2之间存在强烈的负对数相关性（r = -0.952）。在再灌注血流为基线的25%至100%时，左心室功能（速率-压力乘积）与NADH荧光呈负相关（r = -0.922），但在较低的再灌注血流水平时并非如此。恢复收缩功能需要约为基线Do2 25%的明显再灌注阈值。在非常低的再灌注血流（基线的1%）时，确定了另一个阈值血流，此时NADH水平升高超过整体缺血期间观察到的水平（3.4 +/- 3.0%，平均值 +/- 标准误，n = 9），这表明细胞氧化还原状态进一步降低。从灌注液中去除葡萄糖可阻止在基线再灌注血流1%时NADH的增加。在广泛的再灌注Do2值范围内，NADH荧光是心肌细胞氧利用的敏感指标。尽管如NADH变化所示，在非常低的流速下也会利用氧气，但在短期整体缺血后恢复收缩功能需要约为基线Do2 25%的临界阈值。
