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内皮对剪切应力敏感性的抗收缩作用。

Anticonstrictor effect of endothelium sensitivity to shear stress.

作者信息

Melkumyants A M, Balashov S A, Kartamyshev S P

机构信息

Department of Circulation Biomechanics and Control, Institute of Experimental Cardiology, Moscow, Russia.

出版信息

Pflugers Arch. 1994 Jun;427(3-4):264-9. doi: 10.1007/BF00374533.

Abstract

The lumen of arterial vessels is controlled by shear stress at the endothelium; increased shear stress relaxes the smooth muscle thus evoking arterial dilatation. Since shear stress relates directly to flow rate and inversely to the third power of the internal diameter, a decrease in diameter at a constant arterial blood flow augments the shear stress which should result in smooth muscle relaxation counteracting the constriction. This anticonstrictor effect must be stronger the higher the arterial blood flow. To demonstrate the effect of endothelium sensitivity to shear stress on arterial constriction we compared constrictions of endothelium-intact femoral arteries of anaesthetized cats at different blood flow rates. An abrupt decrease in transmural pressure from 120 to 90 or 70 mm Hg at almost zero blood flow rate (where the shear stress mechanism is practically inactive) evoked a fast passive decrease in diameter with further progressive constriction. On the other hand, at flow rates of 8-15 ml/min, after passive constriction the artery began to dilate and the resultant constrictor effect appeared to be considerably smaller than in the virtual absence of flow. Analogously, responses to norepinephrine (3 x 10(-7) or 10(-6) M) were smaller the higher the blood flow. The difference in the magnitudes of the responses at different flow rates was precisely equal to the value calculated using the experimental data characterizing the diameter/flow rate relation. Endothelium removal abolished the dependence of the magnitude of the constrictor responses on blood flow. These data suggest that the endothelium sensitivity to shear stress provides considerable inhibition of arterial constrictor responses, whatever the nature of constrictor stimulus.

摘要

动脉血管的管腔受内皮细胞处的剪切应力控制;剪切应力增加会使平滑肌松弛,从而引起动脉扩张。由于剪切应力与流速成正比,与内径的三次方成反比,在动脉血流恒定的情况下,内径减小会增加剪切应力,这应导致平滑肌松弛,抵消收缩作用。动脉血流越高,这种抗收缩作用就越强。为了证明内皮细胞对剪切应力的敏感性对动脉收缩的影响,我们比较了麻醉猫在不同血流速率下完整内皮的股动脉的收缩情况。在几乎为零的血流速率下(此时剪切应力机制实际上不起作用),跨壁压力从120突然降至90或70 mmHg,会引起直径快速被动减小,并伴有进一步的渐进性收缩。另一方面,在8 - 15 ml/min的血流速率下,被动收缩后动脉开始扩张,最终的收缩效应似乎比实际上无血流时要小得多。类似地,血流越高,对去甲肾上腺素(3×10⁻⁷或10⁻⁶ M)的反应就越小。不同血流速率下反应幅度的差异恰好等于使用表征直径/血流速率关系的实验数据计算出的值。去除内皮消除了收缩反应幅度对血流的依赖性。这些数据表明,无论收缩刺激的性质如何,内皮细胞对剪切应力的敏感性都会对动脉收缩反应产生显著抑制。

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