title: Significance of endogenous opioids in the maintenance of cerebral and spinal vascular CO2-sensitivity in deep hemorrhagic hypotension.
abstract: High CO(2)-sensitivity, one of the major characteristics of the cerebrovascular bed, has been shown to be influenced by a variety of factors. There are no reports, however, on the involvement of the endogenous opioid peptides in the modulation of the CO(2)-sensitivity of the cerebral and spinal cord vessels, either in normotensive or, in hypotensive conditions. The effect of general opiate receptor blockade (1.0mg/kg naloxone, i.v.) on regional cerebrovascular CO(2)-sensitivity was studied with radiolabeled microspheres in 10 distinct brain and spinal cord regions of the anesthetized cat. The CO(2)-induced flow changes were investigated in normotensive, in moderately hypotensive (MAP=80 mmHg) and in deep hypotensive cats (MAP=40 mmHg). The systemic arterial pressure was lowered by hemorrhage. In the normotensive cats, opiate receptor blockade caused no changes in the vascular CO(2)-sensitivity in the investigated cerebral and spinal cord regions. In moderate hypotension, cerebral and spinal CO(2)-sensitivity was significantly reduced by the hemorrhage itself, but remained unaffected by the naloxone administration. In deep hemorrhagic hypotension, however, general opiate receptor blockade resulted not only in a further reduction of the already impaired CO(2)-sensitivity, but even in a reversal of the effect of CO(2) from flow increase to flow decrease. These results indicate that endogenous opioid peptides, which do not seem to influence cerebrovascular reactions in steady-state, normotensive conditions, may contribute significantly to the maintenance of the normal vasodilatory response of the cerebral and spinal cord vessels to CO(2) during hemorrhage-induced deep arterial hypotension.
authors.affiliation: Faculty of Medicine, Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary. sandor@elet2.sote.hu
authors.forename: Peter
authors.initials: P
authors.lastname: Sandor
authors.forename: Martin
authors.initials: M
authors.lastname: Reivich
authors.forename: Katalin
authors.initials: K
authors.lastname: Komjati
mesh_terms: D000818:Animals; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000502:physiology*; D002415:Cats; D002560:Cerebrovascular Circulation / Q000187:drug effects; D005260:Female; D006470:Hemorrhage / Q000150:complications; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D018847:Opioid Peptides / Q000037:antagonists & inhibitors / Q000502:physiology*; D013116:Spinal Cord / Q000098:blood supply / Q000503:physiopathology*
chemical_list: D009292:Narcotic Antagonists; D018847:Opioid Peptides; D002245:Carbon Dioxide; D009270:Naloxone