C E Irazu, E Ruidera, I Singh, J K Orak, C T Fitts, P R Rajagopalan
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引用次数: 0
摘要
在成年大鼠常温缺血30、45、60和90分钟及再灌注24小时后,检测肾组织合成ATP的能力。缺血后ATP合成速率逐渐降低。缺血45分钟时为对照组的64.5%,缺血90分钟后为10.4%。缺血肾脏再灌注24小时可恢复ATP生物合成,以控制缺血肾脏45分钟内的非缺血水平(101.8 +/- 13.9% vs 64.5 +/- 2.5% p < 0.02)。然而,缺血60分钟后,再灌注无影响(59.3 +/- 4.4% vs 51.7 +/- 7.5%),缺血90分钟后再灌注与ATP合成降低相关(10.4 +/- 2.2% vs 3.3 +/- 0.9% p < 0.001)。我们得出结论,当正常缺血间隔时间为45分钟或更短时,线粒体功能通过再灌注恢复。然而,缺血间隔时间超过45分钟会对ATP合成产生不可逆转的损害,缺血90分钟后ATP合成明显减少,这意味着可能过渡到无活力状态。
Effect of ischemia and 24 hour reperfusion on ATP synthesis in the rat kidney.
The ability of renal tissue to synthesize ATP was examined in adult Sprague Dawley Rats immediately following normothermic ischemia of 30, 45, 60 and 90 minutes and upon reperfusion for 24 hours. Following ischemia the rate of ATP synthesis decreased progressively. It was 64.5% of the control at 45 minutes and 10.4% after 90 minutes of ischemia. Reperfusion of the ischemic kidneys for 24 hours restored ATP biosynthesis to control, nonischemic levels in kidneys subjected to ischemia up to 45 minutes (101.8 +/- 13.9% vs 64.5 +/- 2.5% p less than 0.02). However, after 60 minutes of ischemia, reperfusion had no effect (59.3 +/- 4.4% vs 51.7 +/- 7.5%) and reperfusion following 90 minutes of ischemia was associated with decrease ATP synthesis (10.4 +/- 2.2% vs 3.3 +/- 0.9% p less than .001). We conclude that mitochondrial function is restored by reperfusion when normothermic ischemic interval is 45 minutes or less. However, ischemic intervals longer than 45 minutes produce non-reversible impairment of ATP synthesis and the marked reduction following 90 minutes of ischemia signifies possible transition to a non-viable state.