补阳还五汤和益气活血方抗脑缺血再灌注损伤机理的比较研究

比较了补阳还五汤和益气活血方对四血管夹闭模型免缺脑血再灌注损伤的影响，结果发现：１．两方均可明显抑制再灌注后脑组织ＭＤＡ的升高（Ｐ＜０．０５），均可提高脑组织抗氧化酶ＧＳＨ－Ｐｘ活性（Ｐ＜０．０１），提示两方均可对抗再灌注后自由基对脑组织的损伤，保护抗氧化酶，此为两者的共同作用机理之一．２．两方均可抑制再灌注组织ＴＸＢ２的升高（Ｐ＜０．０５），均可提高脑组织６－ｋｅｔｏ－ＰＧＦ１ａ含量（Ｐ＜０．０５），提示调节脑内ＴＸＡ２／ＰＧＩ２平衡为两方另一相同的作用机理。３．补阳还五汤可显著抑制再灌注后脑组织Ｃａ含量的升高（Ｐ＜０．０５），而益气活血方对再灌注后脑组织Ｃａ的升高无明显的影响，提示补阳还五汤可对抗脑缺血再灌后脑细胞的钙超载，此为补阳还五汤与益气活血方作用机理的不同处之一。４．补阳还五汤不能明显抑制再灌注后脑组织ｃＡＭＰ的升高（Ｐ＜０．０５），而注射益气活血方后脑组织ｃＡＭＰ含量升高不甚明显；提示益气活血方对脑组织ＣＡＭＰ的升高具有一定的抑制作用。此为两者作用机理的另一不同之处。

The Comperative Research on the Mechanisms of BYHWTand YQHXF against the Cerebral Ischemic-postischemic Reperfusion injury

his paper researched the effect of Bu Yang Huan Wu Tong (BYHWT) and Yi Qi Hue Xue Fang (YQHXF) onthe cerebral ischemic-postischemic reperfusion injury in the rabbit tetra-vessels obstruct model. The results showed thatthere were the identical and different mechanisms between the two drug recipes above. The identical mechanismsshowed that the two recipes can inhibite the increase of MDA in brain tissue and improve the GSH-Px activity afterreperfusion, which suggested that these drugs own the proteCtive action on the free radical and anti-oxidase, inhibitethe increase of TXB2 and the decline of 6-Keto-PGF1a in brain tissue, which suggested that they might adjust the balance of TXA2/PGI2. The different mechanisms showed that BYHWT can antagonize calcium ion hypercharge in arebral cells induced by the cerebral ischemic-postischemic reperfusion injury and YQHXF can inhibite the increase ofcAMP contents in brain tissue.