Flow-induced responses in skeletal muscle venules: modulation by nitric oxide and prostaglandins.
Flow-induced responses in skeletal muscle venules: modulation by nitric oxide and prostaglandins.
复制标题
DOI：
10.1152/ajpheart.1998.275.3.h831
复制
发表时间：
1998-09
期刊：
影响因子：
--
通讯作者：
A. Koller;G. Dörnyei;G. Kaley
中科院分区：
文献类型：
--
作者：
A. Koller;G. Dörnyei;G. Kaley
骨骼肌小动脉响应于流速/壁切应力（WSS）的增加而扩张。然而，流量/WSS对骨骼肌小静脉直径的影响以及可能的内皮介导的反应尚未得到表征。因此，在内皮去除或应用NO和前列腺素（PG）合成抑制剂N ω-硝基-L-精氨酸（l-NNA，104 M）和吲哚美辛（Indo，2.8 × 105 M）之前和之后，分别测量了加压（10 mmHg）和去甲肾上腺素预收缩（直径179 ± 8 μm）的微静脉直径随灌注液流量增加的变化。灌注液流量增加[由近端和远端插管之间的压差（Pdiff）增加引起]引起，扩张延迟17 ± 2 s，最高流量时达36 ± 9 μm，通过去除/破坏微静脉内皮完全消除了这种反应。WSS的计算表明，在内皮完整的血管中，剪切应力-直径曲线的中点为1.8dyn/cm ~ 2，而在内皮剥脱的血管中，剪切应力随着流量的增加而线性增加，最高可达40 dyn/cm ~ 2。（在14 mmHg Pdiff下从38 ± 11 μm至17 ± 9 μm），而在另外存在Indo的情况下，血流引起小静脉收缩，基底直径减小（在Pdiff 12 mmHg下减小21 ± 8 μm）。因此，在骨骼肌小静脉中，由于灌注液流量增加而导致的剪切应力增加刺激内皮源性NO和PG的释放，从而引起扩张，这反过来又调节WSS，尽管其值低于在小动脉中观察到的值。在没有NO和PG的情况下，显示了流动诱导的收缩，其原因仍然不清楚。从这些数据中，我们提出，小静脉的剪切应力相关的反应参与小静脉阻力的调节，特别是在高流量条件下，如反应性和运动充血。
Skeletal muscle arterioles dilate in response to increases in flow velocity/wall shear stress (WSS). The effect of flow/WSS on the diameter of skeletal muscle venules and the possible endothelial mediation of the response, however, have not yet been characterized. Thus changes in diameter of pressurized (10 mmHg) and norepinephrine-preconstricted venules (179 ± 8 μm in diameter) to increases in perfusate flow before and after endothelium removal or application of inhibitors of NO and prostaglandin (PG) synthesis, N ω-nitro-l-arginine (l-NNA, 104 M) and indomethacin (Indo, 2.8 × 105 M), respectively, were measured. Increases in perfusate flow [elicited by increases in the pressure difference (Pdiff) between proximal and distal cannulas] evoked with a delay of 17 ± 2 s dilations, up to 36 ± 9 μm at the highest flow, a response that was completely eliminated by removal/disruption of the venular endothelium. Calculation of WSS indicated that in endothelium-intact venules, the midpoint of the shear stress-diameter curve was at ∼8 dyn/cm2, whereas in endothelium-denuded vessels, shear stress increased in a linear fashion with increases in flow, up to 40 dyn/cm2.l-NNA significantly reduced flow-induced dilations (from 38 ± 11 to 17 ± 9 μm at 14 mmHg Pdiff), whereas in the additional presence of Indo, flow elicited constriction of venules decreasing basal diameter (by 21 ± 8 μm at Pdiff 12 mmHg). Thus in skeletal muscle venules an increase in shear stress due to increases in perfusate flow stimulates the release of endothelium-derived NO and PGs eliciting dilation, which in turn, regulates WSS, albeit at a lower value than what is observed in arterioles. In the absence of NO and PGs, flow-induced constriction is revealed, the cause of which remains obscure. From these data, we propose that shear stress-related responses of venules are involved in the regulation of venular resistance, especially during high flow conditions, such as reactive and exercise hyperemia.