Ursino M, Fabbri G
Department of Electronics, Computer Science and Systems, Bologna, Italy.
Microvasc Res. 1992 Mar;43(2):156-77. doi: 10.1016/0026-2862(92)90014-g.
The possibility that spontaneous oscillations in microvessel caliber, called vasomotion, arise from the activity of the local myogenic mechanism is analyzed in this work using an original mathematical model. According to experimental results, the model assumes that the myogenic response in microcirculation (transverse arterioles and terminal precapillary-postcapillary microvessels) is characterized by both a static and a dynamic (i.e., rate-dependent) component. Computer simulations demonstrate that the myogenic mechanism of action, thanks to its strong rate-dependent component in terminal arterioles, can produce vascular instability and oscillations of vessel caliber without the need to assume the existence of a local pacemaker in smooth muscle cells. Moreover, these oscillations turn out similar, both in frequency and in shape, to those experimentally observed in microvascular networks. Finally, according to experimental data, several kinds of vasodilatory stimuli (such as arterial hypotension, increase in the tissue metabolic rate, and postischemic reactive hyperemia) cause stoppage of vasomotion and stabilization of vessel caliber.
在这项工作中，我们使用一个原创的数学模型分析了微血管口径的自发振荡（即血管运动）源自局部肌源性机制活动的可能性。根据实验结果，该模型假定微循环（横向小动脉和终末毛细血管前 - 毛细血管后微血管）中的肌源性反应具有静态和动态（即速率依赖性）成分。计算机模拟表明，由于其在终末小动脉中强烈的速率依赖性成分，肌源性作用机制可以产生血管不稳定和血管口径振荡，而无需假定平滑肌细胞中存在局部起搏器。此外，这些振荡在频率和形状上与在微血管网络中实验观察到的振荡相似。最后，根据实验数据，几种血管舒张刺激（如动脉低血压、组织代谢率增加和缺血后反应性充血）会导致血管运动停止和血管口径稳定。
