Abstract

During ischemic events, natural bypass routes such as collateral arterioles can redirect blood flow to the ischemic zone. However, reperfusion of the ischemic arterial tree can also occur in animal models that lack arteriole collaterals, such as Balb/C mice. Collateral capillaries associated with the ischemic arterial tree enlarge and recruit smooth muscle cells in response to an increased pressure gradient. The arterialized collateral capillaries (ACC) must also be able to dilate and constrict in response to the changing metabolic needs of the tissue fed by them. By 21 days after the onset of ischemia, ACCs begin to dilate and constrict in response to physiological stimuli, however it has yet to be shown if the vasodilation of ACCs will increase blood flow in the ischemic arterial tree. To test whether vasodilation of the ACCs will increase blood flow in the ischemic arterial tree, we used laser speckle flowmetry at 21 days post‐ligation of the lateral cranial feed artery of the spinotrapezius muscle. We captured laser speckle images of the entire muscle to determine blood velocities at rest and after application of sodium nitroprusside (SNP). SNP increased blood velocity in the ischemic arterial tree by 60 ± 7% above res2ting velocity. Similarly, in unoperated vasculatures, blood velocity in arterial trees increased by 47 ± 5% above resting velocity. Comparable blood velocity increases between operated and unoperated vasculatures suggest that the ACCs are able to not only increase blood flow to the ischemic arterial tree, but also adequately respond to tissue metabolic demand. These results indicate that supporting the function of ACCs may be a potential therapeutic option for chronic ischemic diseases and their associated complications.

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