The effect of sympathetic stimulation (stellate ganglion) on dog cerebral and cephalic blood flows was studied via a cervical or a thoracic approach to the stellate ganglion under sodium pentobarbital or' chloralose anesthesia. Two different stimulation voltages (3v and 5v) of monophasic pulses were applied for 1 minute. Venous outflow was measured at the confluence of the sagittal, straight and lateral sinuses with the lateral sinuses occluded and with them patent. When the lateral sinuses were occluded, stellate ganglion stimulation resulted in a marked decrease in common carotid blood flow to 38 ± 2.5% (SE) of control and dilation of the ipsilateral pupil, but cerebral blood flow did not change. Similar effects were observed with each of the anatomic approaches, anesthetics, and voltages used and in dogs with low cerebral vascular tone induced by hypercapnia. When the lateral sinuses were kept patent, sympathetic nerve stimulation decreased the venous outflow to 89 ± 2.9% of control and clamping both of the external jugular veins increased venous outflow to 120 ± 2.7% of control. When the lateral sinuses were kept patent and the extracranial venous pressure was increased by clamping both of the external jugular veins, the decrease in venous outflow in response to sympathetic stimulation was even larger: venous outflow was only 65 ± 4.9% of control. We conclude that stimulation of the stellate ganglion has no effect on the cerebral vasculature. Sympathetic stimulation significantly decreases venous blood flow measured at the confluence of the sinuses only when communications between the intracranial and extracranial venous vasculatures are present. KEY WORDS stellate ganglion neural control of brain blood flow vasoconstrictionbrain blood flow autonomic nervous system intracranial vs. extracranial response CO 2 effect on cerebral blood flow• Current experimental evidence supports the concept that cerebral blood vessels and pial arteries are plentifully supplied with adrenergic innervation. It has been shown, however, that the intracranial intraparenchymal arteries and arterioles have only a scanty adrenergic innervation (1-3) compared with the rich innervation of the extraparenchymal vessels (1). This innervation has been well demonstrated by several different techniques: (a) light microscopy (4), (b) electron microscopy (2, 5, 6), and (c) fluorescent histochemistry (7,8). However, the nature and the functional importance of the adrenergic innervation remains
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.
Cerebral venous outflow and carbon dioxide transients were studied during five different transitional states: (1) on and off 10% carbon dioxide breathing, (2) on and off hyperventilation, (3) on 7% carbon dioxide breathing, (4) on 10% carbon dioxide breathing initiated from 7% carbon dioxide breathing, and (5) on 10% carbon dioxide breathing initiated during intracarotid papaverine infusion, in pentobarbital anesthetized, paralyzed, mechanically ventilated dogs. Plots of the temporal relationships between these variables indicated that cerebral blood flow is closely related with cerebral venous carbon dioxide tension but not arterial carbon dioxide tension. The rate at which flow changed upon transition from one steady state to another was phase dependent, in that longer times were required to establish stable conditions in the on phase than in the off phase. The magnitude of the maximum rates of change in cerebral blood flow achieved during transition was influenced both by the size of the forcing function and the level of flow present at the time the response was initiated. Directional changes had no effect upon the maximum rate of the flow change as long as equivalent-sized forcing functions were employed and the initial blood flow levels were similar between responses. However, faster flow transients could be produced by increasing either of the latter two factors. These findings are consistent with the hypothesis that it is either tissue carbon dioxide tension or cerebral venous carbon dioxide tension that is the important variable regulated by cerebral blood flow. The rate-limiting factor in the response appears to be carbon dioxide delivery rate and not the rate of carbon dioxide diffusion.
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