AJP - Heart and Circulatory Physiology, Vol 256, Issue 2 460-H467, Copyright © 1989 by American Physiological Society

ARTICLES

Cervical sympathectomy and cerebral microvascular and blood flow responses to hypocapnic hypoxia

I. Kissen and H. R. Weiss
Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854-5635.

This study evaluated the effects of bilateral superior cervical ganglionectomy on cerebral blood flow (CBF) and utilization of brain capillary reserve in conscious rats during normoxia and hypoxia (8% O2 in N2). Regional CBF was determined in sham-lesioned and ganglionectomized rats with [14C]iodoantipyrine. The percentage of the total volume fraction and number of perfused capillaries was determined by comparing the perfused microvessels, identified by the presence of fluorescein isothiocyanate dextran, with the total microvascular bed, identified by alkaline phosphatase stain. There were no significant differences in regional CBF between control and ganglionectomized rats under normoxic conditions. CBF increased significantly during hypoxia in both control and control ganglionectomized rats. In control, hypoxic flow to caudal structures was significantly higher than to rostral structures and that differential response was prevented by ganglionectomy. There was no significant difference in the number of perfused microvessels between sham-lesioned and ganglionectomized rats during normoxia. The number of perfused arterioles and capillaries was significantly higher under hypoxic conditions than under normoxic conditions in sham and ganglionectomized animals. During hypoxia, the percent of arterioles per squared millimeter perfused increased to 63 +/- 5% in sham-lesioned rats and to a significantly greater extent, 80 +/- 6%, in ganglionectomized rats. The percentage of capillaries per squared millimeter perfused changed similarly. The peripheral sympathetic nervous system appeared to play an important role in the control of cerebral microvascular response to hypoxia.