Delayed postischemic hypoperfusion: evidence against involvement of the noradrenergic locus ceruleus system.
This study explores the possibility that the delayed hypoperfusion observed after an ischemic insult might be due to vasoconstriction induced by the release of noradrenaline from nerves originating in the locus ceruleus. Bilateral 6-hydroxydopamine lesions of the ascending bundles from the locus ceruleus were carried out in the caudal mesencephalon of rats. Local CBF was measured with an autoradiographic technique 60 min following the start of recirculation after incomplete forebrain ischemia. No significant differences in CBF between nonoperated, sham-operated, and noradrenaline-depleted animals were observed in any structure of the forebrain. It is concluded that the noradrenergic locus ceruleus system does not contribute to the development of delayed postischemic hypoperfusion.
D000818:Animals; D001921:Brain / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects; D006892:Hydroxydopamines / Q000494:pharmacology; D002546:Ischemic Attack, Transient / Q000378:metabolism / Q000503:physiopathology*; D008125:Locus Coeruleus / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014018:Tissue Distribution
D006892:Hydroxydopamines; D016627:Oxidopamine; D009638:Norepinephrine