Cerebral venous outflow in the dog; influence of adrenergic and cholinergic substances

¹ Department of Physiology and Pharmacology, Bowman Gray School of Medicine, Wake Forest College, Winston-Salem, North Carolina

In the intact dog, jugular vein outflow markedly decreased during adrenergic stimulation. After occlusion of both jugular bulbs and both vertebral venous sinuses with celloidin and ligation of all collateral communications along the jugular veins, in the orbit and underlying masseter muscle, lateral sinus outflow was not appreciably influenced by intra-arterial injections of 50 µg of epinephrine or arterenol, or by stimulation of the headward end of the severed vasosympathetic trunk, but intra-arterial injections of methacholine caused a weak vasodilator response. It was concluded that, in the dog, prominent communications exist between intra- and extracranial venous structures. Apparent vasoconstrictor responses are due to a reduced contribution to the jugular bulb from extracranial structures and/or to a deflection of some of the cerebral venous blood into channels other than the jugular bulb, as a result of vasoconstriction in the extracranial beds. Vasoconstrictor and cerebral metabolic effects reported in man, using the nitrous oxide technique, might be due similarly to varying contamination of the internal jugular vein blood by blood draining from adrenergically reactive facial vascular beds.

Note:
With the Assistance of Judson Anderson, James Hoyme and George K. Weaver

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