ROLE OF SHEAR-STRESS AND ENDOTHELIAL PROSTAGLANDINS IN FLOW-INDUCED AND VISCOSITY-INDUCED DILATION OF ARTERIOLES INVITRO
ROLE OF SHEAR-STRESS AND ENDOTHELIAL PROSTAGLANDINS IN FLOW-INDUCED AND VISCOSITY-INDUCED DILATION OF ARTERIOLES INVITRO
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DOI：
10.1161/01.res.72.6.1276
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发表时间：
1993-06-01
影响因子：
20.1
通讯作者：
KALEY, G
中科院分区：
文献类型：
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作者：
KOLLER, A;SUN, D;KALEY, G
我们研究了剪切应力变化对大鼠肌离体小动脉直径的影响。在恒定灌注压力（60 mm Hg）下，小动脉的稳态活性直径为80+/-1.2 μ m。血管被动直径（无Ca2+溶液）为156+/-1.8 μ m。剪切应力的变化是由流量（速度）的增加或灌注溶液粘度的增加引起的。在一定的灌注压力下，灌注流量的逐步增加（0-80 mul/min, 10 mul/min）引起直径逐渐增加，延迟几乎等于20秒，最大增加46%。在恒定的20 μ l/min流速下，灌注液粘度的增加（2%、4%和6%葡聚糖[分子量，77,800]）可导致血管逐渐舒张22%。同时改变灌注液的流量和粘度，导致流量-直径曲线向上移动。通过去除小动脉内皮（通过空气）或用吲哚美辛（10(-5)M）抑制血流和黏性引起的扩张。这些抑制治疗的有效性和特异性是用血管活性药物评估的，血管活性药物的作用，关于内皮介导，已经确定。在灌注物的How和/或粘度增加时，小动脉扩张维持计算的壁剪切应力接近控制值，但当扩张被去除内皮或吲哚美辛抑制时，壁剪切应力以累积方式显着增加。我们的结论是，在离体的肌细动脉中，血流的速度或粘度的增加是由于剪应力的增加导致血管舒张剂前列腺素从内皮细胞释放。
We have studied the effect of changes in shear stress on diameter of isolated arterioles of rat cremaster muscle. The steady-state active diameter of arterioles at a constant perfusion pressure (60 mm Hg) was 80+/-1.2 mum. The vessels' passive diameter (Ca2+-free solution) was 156+/-1.8 mum. Changes in shear stress were induced either by an increase in flow (velocity) or by an increase in viscosity of the perfusion solution. At a constant perfusion pressure, the stepwise increase in perfusion flow (0-80 mul/min in 10-mul/min steps) elicited, with a delay of almost-equal-to 20 seconds, a gradual increase in diameter up to 46%. At a constant 20-mul/min flow rate, increases in viscosity of the perfusate (2%, 4%, and 6% dextran [molecular weight, 77,800]) caused a gradual vasodilation up to 22%. Varying flow and viscosity of the perfusate simultaneously resulted in an upward shift of the flow-diameter curve. Both flow- and viscosity-induced dilations were eliminated by the removal of the endothelium of arterioles (by air) or were inhibited by indomethacin (10(-5) M). The efficacy and specificity of these inhibitory treatments were assessed with vasoactive agents whose action, with regard to endothelial mediation, has been determined previously. The arteriolar dilation maintained calculated wall shear stress close to control values during increases in How and/or viscosity of the perfusate, but when the dilation was inhibited by removal of the endothelium or by indomethacin, wall shear stress increased significantly in a cumulative manner. We conclude that, in isolated arterioles of cremaster muscle, the dilation to increased How (velocity) or viscosity of the perfusate is the result of an increase in shear stress that elicits the release of vasodilator prostaglandins from the endothelium.