Shimizu K, Tanaka S, Handa T, Kawazoe S, Arao S, Nakazawa T, Shiraishi M, Asahi T
Nihon Yakurigaku Zasshi. 1983 Dec;82(6):465-74.
Models of post-ischemic acute renal failure were prepared in rats. The effects of adenosine triphosphate-magnesium chloride (ATP-MgCl2) administration following renal ischemia on possible changes in renal function and renal cellular metabolism following ischemia were studied using the model. The results obtained revealed the following: 1) Over 40 minute-renal ischemia led to significant lowerings of renal cellular ATP level and energy charge (EC) by as much as 45 to 57% and 4.1 to 7.4% of the control, respectively, at 90 min following re-establishment of renal blood flow. Significant increases in Na+ in renal tissues were observed, but no changes in K+. Further, lactate level in renal tissues tended to increase with prolonged ischemic time by as much as 27 to 31% of the control, with a renal cellular anaerobic metabolism observed. On the other hand, at 24 hr following recirculation of the kidney, plasma creatinine (P-Cr), blood urea nitrogen (BUN) and fraction excretion of sodium (FENa) increased significantly, and creatinine clearance (C-Cr) and urine osmotic pressure decreased significantly, as compared with the control, indicating ischemic acute renal failure. 2) Intravenous injection of ATP-MgCl2 at a dose of 25 mumole/kg and a rate of 1.0 mumol/min after 40 min of renal ischemia led to significant lowerings of P-Cr, BUN and FENa to 36, 35 and 35% of the control (injected with physiological saline solution), respectively, and to significant elevation of C-Cr and urine osmotic pressure by as much as 41 to 31% of the control respectively, at 24 hr after reperfusion. The above results suggested that the ischemic acute renal failure was caused by the decreases in renal cellular ATP and EC with ischemia, resulting in renal cellular metabolic disturbances. It was further suggested that ATP-MgCl2 administered for such a pathological condition could make significant improvements in renal function.
在大鼠身上制备了缺血后急性肾衰竭模型。使用该模型研究了肾缺血后给予三磷酸腺苷 - 氯化镁（ATP - MgCl2）对缺血后肾功能和肾细胞代谢可能变化的影响。获得的结果如下：1）超过40分钟的肾缺血导致肾血流重建后90分钟时肾细胞ATP水平和能荷（EC）分别显著降低，降至对照组的45%至57%和4.1%至7.4%。观察到肾组织中Na +显著增加，但K +无变化。此外，肾组织中的乳酸水平随着缺血时间延长而趋于增加，最高可达对照组的27%至31%，观察到肾细胞无氧代谢。另一方面，与对照组相比，肾脏再灌注24小时后，血浆肌酐（P - Cr）、血尿素氮（BUN）和钠排泄分数（FENa）显著增加，肌酐清除率（C - Cr）和尿渗透压显著降低，表明发生了缺血性急性肾衰竭。2）肾缺血40分钟后，以25微摩尔/千克的剂量和1.0微摩尔/分钟的速率静脉注射ATP - MgCl2，导致再灌注24小时时P - Cr、BUN和FENa分别显著降低至对照组（注射生理盐水溶液）的36%、35%和35%，C - Cr和尿渗透压分别显著升高至对照组的41%至31%。上述结果表明，缺血性急性肾衰竭是由缺血导致肾细胞ATP和EC降低，进而引起肾细胞代谢紊乱所致。进一步表明，针对这种病理状况给予ATP - MgCl2可显著改善肾功能。
