Koller A, Kaley G
Department of Physiology, New York Medical College, Valhalla 10595.
Am J Physiol. 1991 Mar;260(3 Pt 2):H862-8. doi: 10.1152/ajpheart.1991.260.3.H862.
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 microns; correlation coefficient: r = 0.12, P greater than 0.05) in cremaster muscle of pentobarbital-anesthetized rats. An increase in blood flow velocity (due to parallel arteriolar occlusion) 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 microns), 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 less than 0.05) and during increased flow velocity conditions (r = 0.85, P less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)
在完整内皮存在的情况下,在对照条件下,戊巴比妥麻醉大鼠提睾肌中计算得出的壁面剪切速率(WSR)(均值±标准误:2658±123 s⁻¹;n = 21)与小动脉直径(16.2 - 27.2微米)无关(相关系数:r = 0.12,P>0.05)。血流速度增加(由于并行小动脉阻塞)使WSR显著增加(至4981±253 s⁻¹),随后直径延迟增加(6 - 15秒)(从22.5±0.6微米增至29.5±0.8微米),这导致WSR显著降低(至3879±203 s⁻¹)。由于流速增加和血管扩张,计算得出的小动脉血流量增加了230%。在用轻染技术损伤小动脉内皮后,基础WSR显著升高(3604±341 s⁻¹),尽管WSR增加幅度更大(10360±1471 s⁻¹),但血管扩张并未出现。现在发现,在流速增加前(r = 0.58,P<0.05)和流速增加期间(r = 0.85,P<0.05),小动脉直径与WSR之间均呈负线性相关。此外,内皮受损后本就较低的小动脉血流量在流速增加期间仅增加了66%,因为没有血管扩张。结果表明,壁面剪切应力增加是引发“流量依赖性”小动脉扩张的内皮依赖性机制的刺激因素。(摘要截取自250字)