ENDOTHELIAL REGULATION OF WALL SHEAR-STRESS AND BLOOD-FLOW IN SKELETAL-MUSCLE MICROCIRCULATION
ENDOTHELIAL REGULATION OF WALL SHEAR-STRESS AND BLOOD-FLOW IN SKELETAL-MUSCLE MICROCIRCULATION
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DOI：
10.1152/ajpheart.1991.260.3.h862
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发表时间：
1991-03-01
影响因子：
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通讯作者：
KALEY, G
中科院分区：
文献类型：
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作者：
KOLLER, A;KALEY, G
在内皮完整的情况下，在对照条件下，计算的肌壁切变率(均值+/-SE：2,658+/-123 S-1；n=21)与小动脉直径(16.2-27.2mU-m；相关系数：r=0.12，P>；0.05)无关。血流速度增加(由于平行的小动脉闭塞)导致WSR显著增加(至4,981+/-253 S-1)，然后延迟(6-15 S)直径增加(从22.5+/-0.6至29.5+/-0.8-mU-m)，从而导致WSR显著降低(至3,879+/-203 S-1)。由于血流速度和扩张的增加，计算的小动脉血流量增加了230%。用光染法损伤小动脉内皮后，基础WSR显著升高(3,604+/-341 S~(-1))，尽管WSR增加较多(10,360+/-1,471 S~(-1))，但无扩张作用。现在发现微动脉内径与WSR呈负相关(r=0.58，P<；0.05)，在血流速度增加时(r=0.85，P<；0.05)。此外，内皮受损后已经较少的小动脉血流量在由于没有扩张而血流速度增加的时期只增加了66%。结果表明，壁面切应力的增加是内皮依赖性机制的刺激因素，这种机制引起“血流依赖性”的小动脉扩张。这一机制不仅参与了壁面切应力的负反馈控制，还参与了微循环中阻力和血流的调节。
In the presence of intact endothelium, in control conditions, calculated wall shear rate (WSR) (means +/- SE: 2,658 +/- 123 s-1; n = 21) was independent of arteriolar diameter (16.2-27.2-mu-m; correlation coefficient: r = 0.12, P > 0.05) in cremaster muscle of pentobarbital-anesthetized rats. An increase in blood flow velocity (due to parallel arteriolar occulsion) elicited a significant increase in WSR (to 4,981 +/- 253 s-1) followed by a delayed (6-15 s) increase in diameter (from: 22.5 +/- 0.6 to 29.5 +/- 0.8-mu-m), which consequently resulted in a significant decrease in WSR (to 3,879 +/- 203 s-1). As a result of the increased flow velocity and dilation, calculated arteriolar blood flow increased by 230%. After impairment of the endothelium of arterioles by a light-dye technique, basal WSR became significantly higher (3,604 +/- 341 s-1), and despite a greater increase in WSR (10,360 +/- 1,471 s-1) the dilation was absent. Now an inverse linear correlation was found between arteriolar diameter and WSR both before (r = 0.58, P < 0.05) and during increased flow velocity conditions (r = 0.85, P < 0.05). Also, arteriolar blood flow that was already less after impairment of endothelium increased by only 66% during the period of increased flow velocity due to the absence of dilation. Results suggest that an increase in wall shear stress is the stimulus for the endothelium-dependent mechanism that elicits "flow dependent" arteriolar dilation. This mechanism has a role in the negative-feedback control of wall shear stress and also participates in the regulation of resistance and blood flow in the microcirculation.