EFFECTS OF INTRAVENOUS OR SUBARACHNOID MORPHINE ON CEREBRAL AND SPINAL-CORD HEMODYNAMICS AND ANTAGONISM WITH NALOXONE IN DOGS

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  • 1 January 1983
    • journal article
    • research article
    • Vol. 59  (3) , 175-181
Abstract
In order to elucidate the possible mechanism(s) by which opiates may affect cerebral and spinal circulation and cerebral metabolism, cerebral blood flow (CBF) and spinal cord blood flow (SCBF) were measured simultaneously following i.v. or subarachnoid administration of morphine in dogs lightly anesthetized with halothane. The mean values of CBF and SCBF, using hydrogen clearance methods, were 52.3 .+-. 14.7 ml .cntdot. 100 g-1 .cntdot. min-1 (mean .+-. 1 SD) and 22.3 .+-. 9.0 ml .cntdot. 100 g-1 .cntdot. min-1, respectively. Morphine hydrochloride, 1 mg/kg, when given i.v., reduced both CBF and SCBF to .apprx. 73% of the control values (P < 0.01). These changes were accompanied by decreases in the cerebral metabolic rates for O2 (CMRO2) and glucose (CMRglucose). The circulatory effects and, in part, the metabolic effects, were reversed by naloxone 40 .mu.g/kg i.v. Prior administration of naloxone blocked the morphine effects on CBF and SCBF and suppressed the effects on CMRO2 and CMRglucose. The decreases in blood pressure (MAP) and heart rate (HR) were similar following morphine i.v. with or without prior administration of naloxone. When 0.2 mg morphine was injected into the spinal subarachnoid space, the above variables remained unaffected. Neither naloxone alone, nor its subsequent i.v. administration following spinal morphine, affected cerebral and spinal circulatory or cerebral metabolic indices. Morphine i.v. affects both cerebral and spinal cord blood flow via the opiate receptors at supraspinal sites of action.