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  • Title: Significance of endogenous opioids in the maintenance of cerebral and spinal vascular CO2-sensitivity in deep hemorrhagic hypotension.
    Author: Sandor P, Reivich M, Komjati K.
    Journal: Brain Res Bull; 2003 Feb 15; 59(6):433-8. PubMed ID: 12576139.
    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.
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