Abstract
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 believed 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.
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