On the role of mechanosensitive mechanisms eliciting reactive hyperemia
On the role of mechanosensitive mechanisms eliciting reactive hyperemia
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DOI：
10.1152/ajpheart.00545.2002
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发表时间：
2002-12-01
影响因子：
4.8
通讯作者：
Bagi, Z
中科院分区：
文献类型：
--
作者：
Koller, A;Bagi, Z
我们假设压力（P）和流量（F）等血流动力学的变化对反应性充血的发生有重要影响。为了排除体内因素的影响，使用了分离的大鼠骨骼肌小动脉（类似于 130 只小鼠）。我们发现闭塞后 P 或 P + F 的变化会引发反应性扩张 (RD)。 RD 的峰值（高达 45 mmHg），但 RD 的持续时间，随着闭塞时间（30、60 和 120 秒）的变化而增加到 P 的变化（80 到 10，然后回到 80 mmHg）。然而，P + F (80-10 -80 mmHg + 25-0-25 mul/min) 的变化增加了 RD 的峰值和持续时间（从大约 25 秒增加到 90 秒），且闭塞时间更长。当仅改变P时，一氧化氮合成或内皮去除(E-)的抑制仅降低RD的峰值，而当P+F改变时，RD的峰值和持续时间均降低。钆对拉伸激活的阳离子通道的抑制降低了峰值，但增加了 RD 的持续时间（P 或 P + F），而不受 N-G-硝基-L-精氨酸甲酯 (L-NAME) 或 E- 的影响。当仅 P 发生变化时，金雀异黄素对酪氨酸激酶的抑制会降低 RD 峰值，但不影响 RD 持续时间。然而，当P+F改变时，金雀异黄素降低了RD峰值和持续时间，添加L-NAME降低了RD峰值，但不影响RD持续时间。因此，在孤立的小动脉中，可以产生类似于反应性充血特征的RD，该RD是由变形、拉伸、压力和流动/剪切应力敏感机制引起的，并且部分是由一氧化氮介导的。
We hypothesized that changes in hemodynamic forces such as pressure (P) and flow (F) contribute importantly to the development of reactive hyperemia. To exclude the effects of vivo factors, isolated rat skeletal muscle arterioles (similar to130 mum) were utilized. We found that changes in P or P + F following occlusions elicited reactive dilations (RD). The peak of RD (up to similar to45 mum), but not the duration of RD, increased to changes in P (80 to 10, then back to 80 mmHg) as a function of the length of occlusions (30, 60, and 120 s). However, changes in P + F (80-10 -80 mmHg + 25-0-25 mul/min) increased both the peak and duration of RD (from similar to25 to 90 s) with longer occlusions. When only P changed, inhibition of nitric oxide synthesis or endothelium removal (E-) reduced only the peak of RD, whereas when P + F were changed, both the peak and duration of RD became reduced. Inhibition of stretch-activated cation channels by gadolinium reduced the peak but enhanced the duration of RD (both to P or P + F) that was unaffected by N-G-nitro-L-arginine methyl ester (L-NAME) or by E-. When only P changed, inhibition of tyrosine kinases by genistein reduced peak RD but did not affect the RD duration. However, when P + F changed, genistein reduced both the peak and the duration of RD, additional L-NAME reduced the peak RD, but did not affect the duration of RD. Thus in isolated arterioles an RD resembling the characteristics of reactive hyperemia can be generated that is elicited by deformation, stretch, pressure, and flow/shear stress-sensitive mechanisms and is, in part, mediated by nitric oxide.