Microvascular dilation in response to occlusion: a coordinating role for conducted vasomotor responses.
Microvascular dilation in response to occlusion: a coordinating role for conducted vasomotor responses.
复制标题
DOI：
10.1152/ajpheart.2000.279.1.h279
复制
发表时间：
2000-07
期刊：
影响因子：
--
通讯作者：
K. Dora;D. Damon;B. Duling
中科院分区：
文献类型：
--
作者：
K. Dora;D. Damon;B. Duling
在大鼠提睾微循环中，机械闭塞小动脉分叉的一个分支会导致未闭塞子分支的流量增加和血管舒张。这种扩张归因于微循环中剪切应力依赖性机制的运作。代替或除此之外，我们假设在闭塞期间观察到的扩张是源自闭塞远端的传导信号的结果。为了检验这一假设，我们通过破坏 200 微米的二级或三级小动脉片段中的平滑肌和内皮细胞来阻止传导性血管舒缩反应的上行扩散。我们发现传导阻滞消除或减少了与闭塞相关的通过未闭塞分支的血流增加，并消除或强烈减弱了分支处两条血管的血管舒张反应。我们还注意到，ACh (10(-4) M，0.6 s) 引起的血管舒张会扩散到损伤区域，但不会超出损伤区域。总而言之，这些数据提供了强有力的证据，表明进行的血管舒缩反应在协调血流以应对小动脉闭塞方面具有重要作用。
In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-microm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10(-4) M, 0.6 s) spread to, but not beyond, the area of damage. Taken together, these data provide strong evidence that conducted vasomotor responses have an important role in coordinating blood flow in response to an arteriolar occlusion.