Postischemic augmentation of conducted dilation in cerebral arterioles
Postischemic augmentation of conducted dilation in cerebral arterioles
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DOI：
10.1161/01.str.0000252157.93998.47
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发表时间：
2007-01-01
期刊：
影响因子：
8.3
通讯作者：
Britz, Gavin W.
中科院分区：
文献类型：
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作者：
Ngai, Al C.;Nguyen, Thien-Son;Britz, Gavin W.
背景和目的：血管传导反应可能在脑血管调节中起重要作用，但缺血如何影响这些反应尚不清楚。方法采用线栓法造成大鼠大脑中动脉闭塞（MCAO）模型，分为4组：（A）MCAO 2 h/再灌注24 h组（n = 14），（B）MCAO 2 h/再灌注1h组（n=7），（B）MCAO 2 h/再灌注24 h组（n=14），（C）MCAO 2 h/再灌注24 h组（n=14），（D）MCAO 2 h/再灌注24 h组（n=14），（C）MCAO 2 h/再灌注24 h组（n = 14），（D）MCAO 2 h/再灌注24 h组（n = 14），（D）MCAO 2 h/再灌注24 h组（n= 14）。（C）1小时MCAO/24小时再灌注（n=6）;和（D）1小时MCAO/1小时再灌注（n=5）。在I/R后评估神经功能状态和梗死（2，3，5-氯化三苯基四唑染色）。进行血管舒张反应进行了评估，在大脑中动脉的分支，通过以下的纵向传播的血管舒张或血管收缩，以本地化microapplication的ATP或adenose.Results-Local microapplication的ATP引起的双相收缩（17 3%）和扩张（7 +/- 2%）的反应，而腺苷引起的只有扩张（11 +/- 2%）。这些局部反应沿沿着假手术对照小动脉（1 mm传导距离）纵向传播，并具有快速空间衰减。缺血后24小时再灌注（A组和C组）导致传导性扩张反应显著增强：对ATP的扩张在I/R小动脉中几乎没有衰减。在1小时再灌注组（B和D）中未观察到电导率增加。此外，I/R并没有改变进行constrictions. Conclusions缺血再灌注导致脑小动脉进行血管舒张的特定增强。据推测，增强的电导率可以改善缺血后的脑灌注。
Background and Purpose-Conducted vasomotor responses likely play an important role in cerebrovascular regulation, but it is unclear how these responses may be affected by ischemia. The purpose of this study was to evaluate the hypothesis that cerebral ischemia and reperfusion (I/R) alters vascular conduction in cerebral arterioles.Methods-Middle cerebral artery occlusion (MCAO) was induced by an intraluminal filament technique in 4 groups of rats: (A) 2-hour MCAO/24-hour reperfusion (n=14); (B) 2-hour MCAO/1-hour reperfusion (n=7); (C) I-hour MCAO/24-hour reperfusion (n=6); and (D) 1-hour MCAO/1-hour reperfusion (n=5). Neurological status and infarction (2,3,5-triphenyltetrazolium chloride staining) were evaluated after I/R. Conducted vasomotor responses were assessed in intracerebral branches of the MCA, by following the longitudinal spread of vasodilation or vasoconstriction to localized microapplication of ATP or adenosine.Results-Local microapplication of ATP evoked a biphasic constriction (17 3%) and dilation (7 +/- 2%) response, whereas adenosine elicited only dilation (11 +/- 2%). These local responses spread longitudinally along sham-control arterioles (1 mm conduction distance) with rapid spatial decay. Ischemia followed by 24-hour reperfusion (groups A and C) led to a marked potentiation of conducted dilation responses: dilation to ATP conducted with virtually no decay in I/R arterioles. Augmentation of conductivity was not observed in the 1-hour reperfusion groups (B and D). Moreover, I/R did not alter conducted constriction.Conclusions-Ischemia-reperfusion led to a specific augmentation of conducted vasodilation in cerebral arterioles. Presumably, enhanced conductivity may improve cerebral perfusion after ischemia.