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Using standard in vitro techniques, we found that the canine retroglenoid vein, a vessel that drains a significant fraction of canine cerebral venous effluent, demonstrated the following: an average wall thickness of approximately 240 microns; a norepinephrine (NE) content of approximately 3 micrograms/g tissue; a NE uptake capacity (uptake 1) of approximately 8 nmol/g tissue; an ED50 for NE of 1.9 X 10(-8) M; and a phentolamine-sensitive constriction during electric transmural stimulation that had a median effective frequency of approximately 3 Hz and a maximum response that was approximately 84% of the maximum response to exogenous NE. In a separate series of in vivo experiments conducted in six alpha-chloralose-anesthetized dogs, we found that electrical stimulation of the left superior cervical ganglion produced a phentolamine-sensitive, frequency-dependent increase in cerebral venous pressure (CVP) of up to 19 mm Hg when all cerebral venous effluent was diverted through the left retroglenoid vein. Taken together, our findings suggest that the canine retroglenoid vein undergoes a marked vasoconstriction during physiological frequencies of electric sympathetic nerve stimulation in vivo. Although our data further suggest that the retroglenoid is not a dominant influence on CVP in the intact dog, they do encourage a cautious interpretation of cerebral venous outflow data obtained with techniques in which cerebral effluent is drained primarily by extracranial veins.

Retroglenoid Venoconstriction and its Influence on Canine Intracranial Venous Pressures