Crotty T P
Physiology Department, University College, Cork, Ireland.
Med Hypotheses. 1994 Jun;42(6):367-70. doi: 10.1016/0306-9877(94)90154-6.
A hypothesis is presented on the origin of PSD, the dilatation which occurs in an artery distal to a site of stenosis. The fact that turbulent flow is associated with both PSD and with experimentally induced varicosities suggested that similar mechanisms are involved. That is the basis for a proposal that PSD originates as an active dilator response of the artery wall to circulating NE released in excess from a section of the vasa vasorum (VV) network of the affected artery. Turbulence is believe to be the cause of that excess through multiplying the volume of blood and, consequently, the amount of circulating NE flowing from an artery to its VV. There is published evidence that turbulence does increase flow to the VV of an artery and evidence is presented that if norepinephrine is injected rapidly into a small canine muscular artery, with the aim of creating turbulence in the artery, the injection is promptly followed by localised dilator effects in the artery which, overall, is constricted by the drug.
本文提出了一个关于动脉粥样硬化性外周血管病（PSD）起源的假说，PSD是指在狭窄部位远端的动脉中出现的扩张。湍流与PSD以及实验诱导的静脉曲张都有关联，这一事实表明两者涉及相似的机制。这就是以下提议的基础：PSD起源于动脉壁对从患病动脉的血管滋养管（VV）网络的某一段过量释放的循环去甲肾上腺素（NE）的主动扩张反应。湍流被认为是造成这种过量的原因，它通过增加血流量，进而增加从动脉流向其VV的循环NE量。有已发表的证据表明，湍流确实会增加动脉向其VV的血流量，并且有证据表明，如果将去甲肾上腺素快速注入一条小型犬类肌肉动脉以在动脉中制造湍流，注射后动脉会立即出现局部扩张效应，而总体上该动脉会被药物收缩。
