Okano K, Kokudo Y, Okajima K, Hossain M A, Ishimura K, Yachida S, Tsubouchi T, Wakabayashi H, Maeba T, Maeta H
First Department of Surgery, Kagawa Medical School, 1750-1, Ikenobe, Miki-cho, Kita-gun, Kagawa 761-07, Japan.
World J Surg. 1996 Oct;20(8):1069-75. doi: 10.1007/s002689900162.
The effect of antithrombin III (AT III) supplementation on energy status, microcirculation, cytoprotection, and prostacyclin (PGI2) production during and after a period of warm ischemia of the rat liver was investigated. AT III supplementation (250 units/kg) stimulate prostaglandin I2 (PGI2) production from 1 hour after administration, with maximal production observed at 3 hours. Ischemia was induced by occluding the hepatoduodenal ligament for 30 minutes, and experiments were continued for 60 minutes after reperfusion. The rats received AT III (250 units/kg IC) 30 minutes before induction of liver ischemia (AT III group). In the AT III group, recovery of the beta-ATP/inorganic phosphate ratio measured by 31P nuclear magnetic resonance showed significant improvement (p < 0.01), and the recovery of tissue blood flow markedly improved (p < 0.01) compared to the saline-treated group (control group). Leakages of aspartame aminotransferase, alanine aminotransferase, and lactate dehydrogenase were mitigated in the AT III group (p < 0. 05). Ultrastructural alterations of sinusoidal endothelial cells were markedly reduced in the AT III group. The PGI2 level at the end of reperfusion was significantly elevated (p < 0.01) in the AT III group compared to the control group. The results of this study indicated that pretreatment with AT III significantly improved the energy status and microcirculation, as well as histologic damage, after liver ischemia and reperfusion. One of the fundamental effects of AT III might be mediated through the production of prostacyclin.
研究了补充抗凝血酶III（AT III）对大鼠肝脏热缺血期间及之后能量状态、微循环、细胞保护和前列环素（PGI2）生成的影响。补充AT III（250单位/千克）从给药后1小时开始刺激前列腺素I2（PGI2）生成，3小时时观察到生成量最大。通过阻断肝十二指肠韧带30分钟诱导缺血，并在再灌注后持续实验60分钟。在诱导肝脏缺血前30分钟，大鼠接受AT III（250单位/千克腹腔内注射）（AT III组）。在AT III组中，通过31P核磁共振测量的β-ATP/无机磷酸盐比值的恢复显示出显著改善（p<0.01），与生理盐水处理组（对照组）相比，组织血流的恢复明显改善（p<0.01）。AT III组中天冬氨酸氨基转移酶、丙氨酸氨基转移酶和乳酸脱氢酶的泄漏减轻（p<0.05）。AT III组中窦状内皮细胞的超微结构改变明显减少。与对照组相比，AT III组再灌注结束时的PGI2水平显著升高（p<0.01）。本研究结果表明，AT III预处理可显著改善肝脏缺血再灌注后的能量状态、微循环以及组织学损伤。AT III的一个基本作用可能是通过前列环素的生成介导的。
