蝙蝠葛酚性碱抗兔心脑缺血再灌注损伤作用

目的：探讨蝙蝠葛酚性碱抗家兔心脑缺血再灌注损伤的作用及其机制。方法：结扎家兔左冠状动脉前降支及双侧颈总动脉，30min后复灌，制成心脑缺血再灌模型。分别于缺血前10min，缺血2、10、30min，再灌1、10、30、60、120、180、240min时经股动脉取血2mL，再灌240min后立即取出左心室、海马、皮层、小脑。测定血清及各组织中内二醛（MDA)含量和超氧化物歧化酶（SOD）活性。结果：与对照组相比，缺血再灌组（I－R）复灌10min后血清MDA含量显著升高，而SOD活性显著降低（P＜0．05）。与I－R组相比，应用RAMd后，血清MDA含量降低，而SOD活性升高（P＜0．05）。各组织中MDA含量与SOD活性变化与血清中相似。结论：蝙蝠葛酚性碱通过减轻脂质过氧化所造成的损伤及提高SOD活性，对心脑缺血再灌注损伤具有一定的保护作用。

Effect of phenolic alkaloids from Menispermum dauricum on myocardial-cerebral ischemia-reperfusion injury in rabbits

AIM: To explore the mechanism underlying the effect of phenolic alkaloids from Menispermum dauricum (PAMd) on simultaneous myocardial-cerebral ischemia-reperfusion injury in rabbits. METHODS: Both left anterior descending coronary artery and bilateral carotid arteries were occluded to induce myocardial-cerebral ischemia-reperfusion injury in rabbits. At 30 min after ischemia, the occlusion was removed and shed blood was rapidly reinfused. Two mL of blood was taken from femoral artery at 10 min before ischemia, 1, 10, and 30 min after ischemia, and 1, 10, 30, 60, 120, 180, and 240 min after reperfusion. Each rabbit was sacrificed at the end of reperfusion, and left ventricle, hippocampus, cortex, and cerebellum were taken out. Malondial-dehyde (MDA) content and superoxide dismutase (SOD) activity were determined. RESULTS: At 10 min after reperfusion, MDA content in serum was significantly higher and SOD activity was lower in ischemia-reperfusion (I-R) group than those of control group (P < 0.05). After administration of PAMd, MDA content was lower and SOD activity was higher in serum than those of I-R group (P < 0.05). Both MDA content and SOD activity in tissues had the similar results with those in serum. CONCLUSION: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus PAMd might play a protective role in simultaneous myocardial-cerebral ischemia-reperfusion injury.