Key result
Carotid bifurcation denervation increases arterial pressure by ~26 mmHg without altering cerebral autoregulation.
Demonstrates that carotid baroreceptors are not required for cerebral blood flow autoregulation in dogs, indicating independent local vascular control.
Cerebral venous outflow was measured in anesthetized dogs at the confluence of the sagittal and straight sinuses, with the lateral sinuses occluded. Denervation of the carotid bifurcation increased systemic arterial pressure (+25.8; SE ±7.7 mm Hg) and decreased cerebral vascular conductance (-0.018; SE ±0.005 ml/min · mm Hg); stimulation of the carotid sinus nerve decreased systemic arterial pressure and increased cerebral vascular conductance. Graded constrictions of the common carotid arteries induced transient responses of the cerebral blood flow that were characteristic of an autoregulatory process. Plots of the steady-state pressures and flows during the decreases of perfusion pressure were concave toward the pressure axis, were similar before and after denervation of the carotid bifurcation, and were indicative of autoregulation. We conclude that pressoreceptors in the carotid bifurcation or other pressoreceptors in systemic vessels upstream from the carotid bifurcation are not necessary for the control of the "tone" of the cerebral vasculature or in the mechanism of the autoregulation of cerebral blood flow.
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Rapela et al. (1967) studied Autoregulation of cerebral blood flow. Carotid bifurcation denervation, carotid sinus nerve stimulation, and graded common carotid artery constriction vs. Before denervation was evaluated on Systemic arterial pressure, cerebral vascular conductance, and cerebral blood flow autoregulation. Carotid bifurcation denervation raised arterial pressure (+25.8±7.7 mmHg) and reduced cerebral conductance (-0.018±0.005 ml/min·mmHg) without altering autoregulation.
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