Rapid tolerance to focal cerebral ischemia in rats is attenuated by adenosine A1 receptor antagonist
Rapid tolerance to focal cerebral ischemia in rats is attenuated by adenosine A1 receptor antagonist
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DOI：
10.1097/00004647-200202000-00004
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发表时间：
2002-02-01
影响因子：
6.3
通讯作者：
Sakabe, T
中科院分区：
文献类型：
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作者：
Nakamura, M;Nakakimura, K;Sakabe, T
两种类型的脑缺血耐受性，快速和延迟，已被报道的条件抗试验损伤之间的时间间隔。虽然许多报道表明，延迟相神经保护诱导预处理是明显的1周或更长时间后，有一些研究快速诱导的耐受，和报告的神经保护作用变得模糊7天后的侮辱。作者研究了在大鼠局灶性缺血模型中再灌注7天后是否存在这种快速缺血耐受，并研究了腺苷A受体拮抗剂DPCPX（8-环戊基-1，3-二丙基黄嘌呤）的调节作用。大脑中动脉闭塞30分钟的预处理在1小时再灌注后给予180分钟的局灶性缺血后7天减少了梗死体积。快速预处理也改善了神经功能结局。这些有益的效果减弱预处理的0.1毫克/公斤的DPCPX，不影响梗死体积后，空调（30分钟）或测试（180分钟）缺血时，单独给药。结果表明，短暂局灶性缺血预处理可诱导对随后严重缺血损伤的快速耐受，再灌注7天后这种效应仍然存在，并且快速缺血耐受可能通过腺苷A（1）受体相关机制介导。
Two types of ischemic tolerance in the brain, rapid and delayed, have been reported in terms of the interval between the conditioning anti test insults. Although many reports showed that delayed-phase neuroprotection evoked by preconditioning is evident after 1 week or longer, there have been a few investigations about rapidly induced tolerance, and the reported neuroprotective effects become ambiguous 7 days after the insults. The authors examined whether this rapid ischemic tolerance exists after 7 days of reperfusion in a rat focal ischemic model, and investigated modulating effects of the adenosine A, receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropytxanthine). Preconditioning with 30 minutes of middle cerebral artery occlusion reduced infarct volume 7 days after 180 minutes of subsequent focal ischemia given after 1-hour reperfusion. The rapid preconditioning also improved neurologic outcome. These beneficial effects were attenuated by pretreatment of 0.1 mg/kg DPCPX, which did not influence the infarct volume after conditioning (30 minutes) or test (180 minutes) ischemia when given alone. The results show that preconditioning with a brief focal ischemia induces rapid tolerance to a subsequent severe ischemic insult, the effect of which is still present after 7 days of reperfusion, and that the rapid ischemic tolerance is possibly mediated through an adenosine A(1) receptor-related mechanism.