title: Adaptation of the cerebrocortical circulation to carotid artery occlusion involves blood flow redistribution between cortical regions and is independent of eNOS.
abstract: Cerebral circulation is secured by feed-forward and feed-back control pathways to maintain and eventually reestablish the optimal oxygen and nutrient supply of neurons in case of disturbances of the cardiovascular system. Using the high temporal and spatial resolution of laser-speckle imaging we aimed to analyze the pattern of cerebrocortical blood flow (CoBF) changes after unilateral (left) carotid artery occlusion (CAO) in anesthetized mice to evaluate the contribution of macrovascular (circle of Willis) vs. pial collateral vessels as well as that of endothelial nitric oxide synthase (eNOS) to the cerebrovascular adaptation to CAO. In wild-type mice CoBF reduction in the left temporal cortex started immediately after CAO, reaching its maximum (-26%) at 5-10 s. Thereafter, CoBF recovered close to the preocclusion level within 30 s indicating the activation of feed-back pathway(s). Interestingly, the frontoparietal cerebrocortical regions also showed CoBF reduction in the left (-17-19%) but not in the right hemisphere, although these brain areas receive their blood supply from the common azygos anterior cerebral artery in mice. In eNOS-deficient animals the acute CoBF reduction after CAO was unaltered, and the recovery was even accelerated compared with controls. These results indicate that 1) the Willis circle alone is not sufficient to provide an immediate compensation for the loss of one carotid artery, 2) pial collaterals attenuate the ischemia of the temporal cortex ipsilateral to CAO at the expense of the blood supply of the frontoparietal region, and 3) eNOS, surprisingly, does not play an important role in this CoBF redistribution.
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and.
authors: Andreas
authors: A
authors: Polycarpou
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and.
authors: László
authors: L
authors: Hricisák
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and Max Planck Institute for Heart and Lung Research, Department of Pharmacology, Bad Nauheim, Germany.
authors: András
authors: A
authors: Iring
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and.
authors: Daniel
authors: D
authors: Safar
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and.
authors: Éva
authors: É
authors: Ruisanchez
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and.
authors: Béla
authors: B
authors: Horváth
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and.
authors: Péter
authors: P
authors: Sándor
authors: Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary; and benyo.zoltan@med.semmelweis-univ.hu.
authors: Zoltán
authors: Z
authors: Benyó
mesh_terms: D000222:Adaptation, Physiological / Q000235:genetics / Q000502:physiology*; D000818:Animals; D002340:Carotid Artery Diseases / Q000503:physiopathology*; D017536:Carotid Artery, Common / Q000601:surgery*; D002540:Cerebral Cortex / Q000098:blood supply*; D002560:Cerebrovascular Circulation / Q000235:genetics / Q000502:physiology*; D002941:Circle of Willis; D003097:Collateral Circulation; D006439:Hemodynamics; D008026:Ligation; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D010841:Pia Mater / Q000098:blood supply; D013702:Temporal Lobe / Q000098:blood supply
chemical_list: D052250:Nitric Oxide Synthase Type III; C496315:Nos3 protein, mouse
keywords: carotid artery occlusion; cerebrocortical microcirculation; cerebrovascular regulation; eNOS; pial collateral circulation