Moderate cerebral venous congestion induces rapid cerebral protection via adenosine A1 receptor activation
Moderate cerebral venous congestion induces rapid cerebral protection via adenosine A1 receptor activation
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DOI：
10.1016/j.brainres.2006.09.019
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发表时间：
2006-11-29
期刊：
影响因子：
2.9
通讯作者：
Aoyai, Shigeaki
中科院分区：
文献类型：
--
作者：
Akaiwa, Keiichi;Akashi, Hidetoshi;Aoyai, Shigeaki
中风是心血管手术中一种破坏性的并发症，脑静脉循环障碍（CVCD）引起的颅内压升高会加剧神经元损伤。然而，我们之前报道过脑缺血前的CVCD减少了梗塞面积。在本研究中，通过颈动脉插入细丝，在自发性高血压大鼠中诱导局灶性脑缺血。将大鼠分为以下四组：假手术组、轻度或重度静脉充血（VC）组和 DPCPX。 DPCPX 组在轻度 VC 之前接受腺苷 A1 受体拮抗剂 8-环戊基-1,3-二丙基黄嘌呤 (DPCPX)。对四组的行为、梗塞体积、水肿和 S-100 蛋白进行评估。轻度VC和重度VC组的梗死体积率显着低于假手术组和DPCPX组。然而，严重VC组的死亡率随着时间的推移而恶化。我们观察到，与 DPCPX 组相比，轻度 VC 组的水肿显着减轻。行为评分还表明，轻度 VC 组的神经功能缺损少于其他三组（包括 DPCPX 组）。通过在脑缺血前给予适当程度的 VC，我们能够通过腺苷 A1 受体激活来诱导快速脑保护。大脑中动脉闭塞所致。我们的工作提出了这种有效的 VC 可能导致脑保护和腺苷 A1 受体激活的可能机制。 (c) 2006 Elsevier B.V. 保留所有权利。
Stroke is a devastating complication in cardiovascular surgery, and neuronal damage is worsened by intracranial pressure elevation caused by cerebral venous circulatory disturbances (CVCD). However, we have previously reported that CVCD before cerebral ischemia decreases the infarct area. In the present study, focal cerebral ischemia was induced in spontaneously hypertensive rats by filament insertion through the carotid artery. Rats were divided into the following four groups: sham-operated, mild or severe venous congestion (VC), and DPCPX. The DPCPX group received the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) prior to mild VC. Behavior, infarct volume, edema and S-100 protein were evaluated among the four groups. The infarct volume rates in mild VC and severe VC groups were significantly less than that in sham-operated and DPCPX groups. However, the mortality of the severe VC group worsened in a time-dependent manner. We observed a significant decrease in edema in the mild VC group compared to the DPCPX group. Behavioral scores also indicated that the mild VC group had fewer neurological deficits than the other three groups, including the DPCPX group. We were able to induce rapid cerebral protection via adenosine A1 receptor activation by administering an appropriate degree of VC prior to cerebral ischemia. produced by middle cerebral artery occlusion. Our work suggests possible mechanisms by which such effective VC may lead to cerebral protection and adenosine A1 receptor activation. (c) 2006 Elsevier B.V. All rights reserved.