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目的探讨不同的血压诱导方式对大鼠急性永久性脑缺血后神经保护作用的机制。方法雄性SD大鼠32只,随机分为4组,对照组(n=8)、早期诱导血压升高组(n=8)、诱导血压降低组(n=8)、晚期诱导血压升高组(n=8)。采用线拴法制备永久性脑缺血大鼠模型,分别在脑缺血3h后药物诱导血压升高、3h后诱导血压降低、18h后诱导血压升高。在缺血24h时观察大鼠的神经功能评分以及脑梗死体积情况。结果脑缺血24h时,早期血压升高组较对照组梗死体积明显减少(P<0.05),血压降低组梗死体积最大(P<0.05),晚期血压升高组梗死体积和对照组相比没有统计学意义(P>0.05)。早期血压升高组大鼠的神经功能评分明显改善(P<0.05)。结论升高血压明显比降低血压能够减少急性永久性脑缺血大鼠梗死体积,改善神经功能。早期诱导血压升高比晚期诱导血压升高更具有神经保护作用。
Objective To explore the mechanism of different blood pressure induction on neuroprotective effect after acute permanent cerebral ischemia in rats. Methods Thirty-two male SD rats were randomly divided into 4 groups: control group (n = 8), early induced hypertension (n = 8), induced hypotension (n = 8), late induced hypertension (n = 8). The model of permanent cerebral ischemia was established by the tethering method. After 3h of cerebral ischemia, the drug-induced blood pressure was increased, the blood pressure was decreased after 3h, and the blood pressure was increased after 18h. Neurological deficit scores and cerebral infarct volume were observed at 24h of ischemia. Results Compared with the control group, infarction volume decreased significantly (P <0.05) and infarction volume decreased significantly (P <0.05) in the early stage of high blood pressure group at 24 hours after cerebral ischemia. Compared with the control group, Statistical significance (P> 0.05). The neurological scores of the rats with early hypertension were significantly improved (P <0.05). Conclusion It is concluded that increasing blood pressure significantly reduces infarction volume and improving neurological function in acute permanent cerebral ischemia rats compared with decreasing blood pressure. Early induction of blood pressure induced by higher than the late induction of a more neuroprotective effect.