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Effects of middle cerebral artery occlusion on the conduction of vasomotor responses along rat cerebral arterioles
Author(s) -
Ngai Al C,
Nguyen ThienSon K,
Meno Joseph R.,
Britz Gavin
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a276-c
Subject(s) - vasomotor , medicine , middle cerebral artery , cerebral arteries , occlusion , cardiology , cerebral circulation , anatomy , anesthesia , ischemia
Vascular communication mechanisms, such as conducted vasomotor responses, likely play an important role in cerebrovascular regulation, but it is unclear how these mechanisms may be affected by ischemia. In this study, we determined the effect of focal cerebral ischemia on the conducted vasomotor responses of intracerebral arterioles to ATP and to adenosine (Ado). After 2‐ hours of middle cerebral artery occlusion (MCAO) and a 24‐hour reperfusion period in Sprague Dawley rats, intracerebral branches of the MCA were isolated and cannulated with a concentric micropipette system. Both ischemic (n=13) and sham‐control (n=8) arterioles developed similar myogenic tone (~70% of passive diameter, 60 mmHg). Pressure‐pulse application of Ado (10 mM) and ATP (5 mM) induced both a direct local response, and a secondary conducted response that spread longitudinally along the vessel. ATP caused a local biphasic response of constriction (17±2%) followed by dilation (7±3%), whereas Ado elicited only dilation (13±2%). In sham‐control vessels, the constriction/dilation responses to ATP markedly decreased (71%/57%) over a 1 mm distance. Ado‐induced dilation decayed even more rapidly and was undetectable at 1 mm. In ischemic vessels, the decay of ATP‐induced constriction (70%) was similar to that in sham‐controls. On the other hand, dilation responses to either ATP or Ado conducted with virtually no decay in ischemic arterioles over the same distance. We conclude that ischemia‐reperfusion led to a specific upregulation of conducted vasodilaton in rat cerebral arterioles. Funded by AHA Grant 0255703N.