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      Postischemic Cerebral Blood Flow and Neuroeffector Mechanisms


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          The influence of neuroeffector mechanisms in the regulation of postischemic cerebral blood flow was investigated by microsphere determination in 8 cats after chronic unilateral vascular deafferentation by trigeminal ganglionectomy. The animals were subjected to 90 min of reperfusion following 10 min of global ischemia induced by 4-vessel occlusion and systemic hypotension. Cortical hyperemia 30 min after reperfusion was attenuated by up to 48% in cortical gray matter ipsilateral to the side of trigeminal ganglionectomy (p < 0.01). Axon reflex mechanisms involving the release of neuropeptides from peripheral sensory nerve fibers, such as substance P (SP), calcitonin gene-related peptide (CGRP) and neurokinin A (NKA), mediate this response. SP and NKA cause vasodilation by endothelium-dependent mechanisms (endothelium-dependent relaxing factor), whereas CGRP relaxes vascular smooth muscle by direct receptor interactions. Studies were therefore undertaken to determine the extent to which endothelium-dependent mechanisms mediate the hyperemia following global cerebral ischemia. In 7 intact cats, the postischemic response of pial arterioles to the topical application of acetylcholine (ACh; 10<sup>–7</sup> M), an endothelial-dependent vasodilator, was measured using a closed cranial window technique. Although ACh increased pial arteriolar caliber by 17 % under resting conditions, the same dose elicited a vasoconstrictor response (87% of pre-ACh diameter 30 min after reperfusion) for the first 60 min of reperfusion after 10 min of ischemia. ACh-induced vasodilation was restored by 75 min (105%), but was less than control even at 120 min (109 vs. 117%; p < 0.05). The ability of sensory denervation to attenuate cortical hyperemia, combined with the demonstrated loss of endothelium-dependent vasodilation during the early postischemic period, indicates that CGRP, a nonendothelium-dependent vasodilator, is a likely mediator of postischemic hyperperfusion.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 28
          : 1-3
          : 46-51
          aStroke Research Laboratory, Neurology and Neurosurgery Services, Massachusetts General Hospital, Harvard Medical School, Boston, Mass.; bDivision of Cardiology, Department of Medicine, Medical College of Virginia, Richmond, Va., USA
          158842 Blood Vessels 1991;28:46–51
          © 1991 S. Karger AG, Basel

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          Page count
          Pages: 6
          Neuronal Control of Vascular Function


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