Sympathetic effect on cerebral blood flow regulation in hypoxic newborn lambs

Abstract

A study was made to determine whether adrenergic stimulation during hypoxia modulates total or regional cerebral blood flow (CBF) in the newborn lamb. CBF was determined with the tracer microsphere technique (15-.mu.m diameter) in 17 unanesthetized, mechanically ventilated lambs during normoxia [arterial O2 tension (PaO2) 84 .+-. 3 mmHg] and following 20 min of isocapnic hypoxia (PaO2 24 .+-. 2 mmHg). Nine of the lambs were pretreated with the postsynaptic .alpha.-antagonist prazosin HCl (0.5 mg/kg i.v.), while 8 lambs received an equal volume of saline and served as controls. Total CBF was 110 .+-. 4 ml .cntdot. min-1 .cntdot. 100 g-1 and increased to 226 .+-. 18 during hypoxia in the control group. In the .alpha.-blocked lambs, mean arterial blood pressure and cerebrovascular resistance (CVR) decreased during normoxia; CBF was not altered. During hypoxia, CBF increased to 196 .+-. 23 ml .cntdot. min-1 .cntdot. 100 g-1 in the .alpha.-blocked group; CVR during hypoxia was not different from the control group (0.40 .+-. 0.03 and 0.37 .+-. 0.04 mmHg .cntdot. ml-1 .cntdot. min-1 .cntdot. 100 g in control, and .alpha.-blocked lambs, respectively). Regional blood flow to the cerebrum, caudate nucleus, hippocampus, thalamus-hypothalamus, midbrain, pons, medulla and cerebellum were also unaffected by .alpha.-blockade. In another group of lambs, the efficacy of .alpha.-blockade by prazosin was tested. In 4 anesthetized hypoxic (PaO2 23-27 mmHg) lambs, unilateral electrical stimulation of the superior cervical sympathetic ganglion reduced total CBF by 25 .+-. 3%, and this effect was attenuated by .alpha.-blockade with prazosin. The data demonstrate a functionally developed sympathetic innervation of the cerebral vasculature in newborn lambs, the effect of which can be blocked by prazosin. The cerebrovascular response to hypoxia was not altered by blockade of these nerves in awake animals, suggesting that reflex sympathetic activation is not a factor in the regulation of total or regional CBF during hypoxia.