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目的:观察新生SD大鼠缺血缺氧性脑损伤(HIBD)后脑组织内环磷腺苷水平(cAMP)的变化及初步探讨环磷腺苷葡胺(MCA)对新生SD大鼠缺血缺氧性脑损伤的干预作用。方法:建立新生大鼠HIBD模型,于缺血缺氧后2、24、48、72、168 h(7天)时测定脑组织cAMP的含量;观察用MCA 24、48、72 h后脑组织内cAMP含量以及72 h后脑组织含水量,大脑损伤程度,超氧化物歧化酶活性(SOD)及氧化代谢产物丙二醛(MDA)含量以及脑组织病理学变化。结果:新生大鼠缺血缺氧后脑组织cAMP含量显著下降,缺氧后2 h脑组织内cAMP水平下降最显著(至正常的25%左右),7天后仍低于正常水平(达70%左右);用MCA后,脑组织cAMP水平显著升高,脑组织含水量和脑损伤程度、MDA下降,SOD活性升高,病理变化减轻。结论:缺血缺氧后脑组织内cAMP代谢紊乱,早期给予外源性cAMP类药物对缺血缺氧性脑损伤具有一定的保护作用,提示cAMP代谢紊乱可能参与缺血缺氧脑损伤的病理机制。
Objective: To observe the changes of cAMP in brain tissue of neonatal SD rats after hypoxic-ischemic brain damage (HIBD) and to investigate the effect of cyclic adenosine monophosphate (MCA) Oxygen brain injury intervention. Methods: HIBD model was established in neonatal rats. The levels of cAMP in brain tissue were determined at 2, 24, 48, 72, 168 h after hypoxia (7 days). The levels of cAMP , Brain water content, brain damage degree, SOD activity and malondialdehyde (MDA) content and brain histopathological changes after 72 h. Results: The content of cAMP in brain tissue of hypoxic-ischemic-reoxygenation rats decreased significantly, and the level of cAMP decreased most significantly (normal 25%) 2 h after hypoxia, and still below the normal level 7 days later (up to 70%) ); After MCA, cAMP level in brain tissue was significantly increased, brain water content and brain injury, MDA decreased, SOD activity increased, pathological changes alleviated. CONCLUSION: Cerebral cAMP metabolism is disturbed after hypoxia and hypoxia, and early administration of exogenous cAMP has some protective effects on hypoxic-ischemic brain damage, suggesting that cAMP metabolism may be involved in the pathogenesis of hypoxic-ischemic brain damage .