[Protective effect of phenolic alkaloids from Menispermum dauricum on myocardial cerebral ischemia/reperfusion injury in rabbits].
Fang Wang, Gang Zhao, Qing Lü, Ling Qu, Lianjun Guo
Abstract
Fang Wang, Gang Zhao, Qing Lü, Ling Qu, Lianjun Guo
Abstract
OBJECTIVE: To explore the mechanism underlying the effects of phenolic alkaloids abstracted from Menispermum dauricum(PAMd) on concurrent myocardial and cerebral ischemia/reperfusion injury in rabbits. METHODS: Both left anterior descending coronary artery and bilateral carotid arteries were ligated to induce myocardial and cerebral ischemia/reperfusion injury at the same time in rabbits. At 30 minutes after ischemia, the occlusion was released to allow return of circulation, and 2 ml of blood was collected from the femoral vein 10 minutes before ischemia, 1, 10, 30 minutes after ischemia, and 1,10, 30, 60, 120, 180, 240 minutes after reperfusion. All rabbits were sacrificed at the end of reperfusion, and the left ventricle, hippocampus, cortex, and cerebellum were removed for examination. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. RESULTS: At 10 minutes after reperfusion, MDA content in serum was significantly higher and SOD activity was significantly lower in ischemia/reperfusion group than those of control group (both P<0.05). In rabbits with administration of PAMd, MDA content was lower and SOD activity was higher in serum compared with ischemia/reperfusion group(P<0.05). Similar results as in the blood in regard to MDA content and SOD activity were obtained in tissues. CONCLUSION: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus it might play a protective role in concurrent myocardial-cerebral ischemia/reperfusion injury.
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OBJECTIVE: To explore the mechanism underlying the effects of phenolic alkaloids abstracted from Menispermum dauricum(PAMd) on concurrent myocardial and cerebral ischemia/reperfusion injury in rabbits. METHODS: Both left anterior descending coronary artery and bilateral carotid arteries were ligated to induce myocardial and cerebral ischemia/reperfusion injury at the same time in rabbits. At 30 minutes after ischemia, the occlusion was released to allow return of circulation, and 2 ml of blood was collected from the femoral vein 10 minutes before ischemia, 1, 10, 30 minutes after ischemia, and 1,10, 30, 60, 120, 180, 240 minutes after reperfusion. All rabbits were sacrificed at the end of reperfusion, and the left ventricle, hippocampus, cortex, and cerebellum were removed for examination. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. RESULTS: At 10 minutes after reperfusion, MDA content in serum was significantly higher and SOD activity was significantly lower in ischemia/reperfusion group than those of control group (both P<0.05). In rabbits with administration of PAMd, MDA content was lower and SOD activity was higher in serum compared with ischemia/reperfusion group(P<0.05). Similar results as in the blood in regard to MDA content and SOD activity were obtained in tissues. CONCLUSION: PAMd could attenuate the injury induced by lipid peroxidation and enhance the activity of SOD, thus it might play a protective role in concurrent myocardial-cerebral ischemia/reperfusion injury.
Key concepts: Medicine, Ischemia, Malondialdehyde, Reperfusion injury, Anesthesia, Lipid peroxidation, Superoxide dismutase, Venous blood