Abstract
Native collateral vessels creates a natural bypass for blood flow around an arterial occlusion, potentially mitigating the effects of ischemic diseases, such as peripheral arterial occlusive disease in which arterial stenosis restricts blood flow to the limbs. Unfortunately, not all patients have robust collateral networks; however, animal models lacking native collaterals demonstrate the ability to adapt to the ischemic environment through arterialization of collateral capillaries, reperfusing the ischemic zone. Reactivity is important for normal muscle function in these developed vessels because increased metabolic demand is only satisfied when blood vessels can dilate to increase flow. Understanding cellular mechanisms behind impaired vasodilation is key to identifying potential therapeutic targets for improving reactivity. To assess vascular reactivity, the lateral cranial spinotrapezius feed artery was ligated 7 days prior to the application of endothelial‐dependent (acetylcholine, ACh) and endothelial‐independent (sodium nitroprusside, SNP) vasodilators. Although arterialized capillaries dilated significantly in response to ACh and SNP, dilation was impaired when compared to equivalent‐diameter terminal arterials on the sham side (19.0 ± 3.6% vs. 69.5 ± 14.0% and 20.0 ± 4.9% vs. 95.7 ± 9.2%, respectively). This impairment can be attributed to smooth muscle cell dysfunction because the responses to ACh and SNP are similar. To determine if other smooth muscle‐dependent vasodilatory pathways are also impaired, hydrogen sulfide and papaverine were applied using the same methods (31.3 ± 16.6% vs. 97.1 ± 16.2% and 49.0 ± 8.8% vs. 86.3 ± 6.1%). Future work will further characterize the signaling cascades described herein.
Published Version
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