Role of the carotid body in speeding the cerebrovascular response to altered PaCO2 in baboons.

Abstract

SUMMARYThe alterations in cerebral perfusion with graded hypercapnia were measured in the baboon using the intra-carotid 1M xenon clearance technique. In addition, the tidal percent of COj and the blood flow in the common carotid artery were measured using a capnograph and an electromagnetic flowmeter respectively. The delay times between the induced increments in tidal respiratory percent of CO] and the beginning of the blood flow increments were assessed, together with the rate of increment of the blood flow at each level of hypercapnia. The changes in cerebral perfusion, delay time and rate of blood flow increase with hypercapnia were measured before and after bilateral denervation and destruction of the carotid bifurcation receptors.Hypercapnia normally caused an increased cerebral perfusion which was attenuated when carotid receptor function was destroyed. This change was only significantly different from normal with the highest value of Pco a . Before removal of carotid receptor function the mean delay time was 13.7 ± 1.2 seconds and the rate of increment in carotid flow was 29.7 ± 8.4 ml/min per min. These values were similar at all levels of hypercapnia. After carotid receptor removal the mean delay time was significantly increased at 35.8 ± 9.0 seconds while the rate of flow increment was unchanged at 36.0 ± 5.2 ml/min per min. These results in the baboon suggest that the carotid bifurcation receptors provide a quantitatively small but fast mechanism mediating the cerebrovascular dilator response to hypercapnia. IN 1974, Ponte and Purves1 suggested that the cerebral vasodilator response to a raised arterial Pco 2 is mediated, at least in part, by carotid and aortic chemoreceptors. Since then many workers have investigated the role of a neural reflex in cerebral hypercapnic vasodilatation. Hoff, Mackenzie and Harper 2 showed that, in the baboon, section of the seventh cranial nerve had no effect on the cerebral response to either hypercapnia or hypoxia. Similarly, Linton, Miller and Cameron 3 found in the rabbit that the carotid sinus had no influence on the response to hypercapnia. Other recent studies also failed to demonstrate any role for the carotid chemoreceptors in the control of cerebral blood flow in the dog* or cat. 6 On the other hand, James and MacDonell 6 have shown in the dog that stimulation of the vascularly isolated carotid bifurcation with hypercapnic or hypertensive blood caused alteration in cerebral blood flow. We have recently shown that the carotid body chemoreceptors do play a quantitatively small role in the cerebrovascular dilator response to hypercapnia.7 However, this role became apparent only at high Paco 2 values and was quantitatively smaller than that reported previously by Ponte and Purves.1 Also, we have suggested that the hypercapnic cerebral vasodilatation is mediated by a quantitatively small but fast reflex arising in the peripheral chemoreceptors.7 If this is true, it may explain some of the variation in the literature as different authors may have made their measur...

Carotid body denervation in dogs: eupnea and the ventilatory response to hyperoxic hypercapnia

“…More explicitly, if increases in CO 2 at the carotid body cause reflex increases in sympathetic outflow that reduce brain blood flow, then CBX would eliminate this reflex sympathetic outflow, allowing for greater increases in brain blood flow during the rebreathe tests, which would blunt the rise in brain tissue PCO 2 compared with the intact responses. It is unlikely, however, that this mechanism explains our findings because it has been demonstrated that CBX does not affect the cerebral blood flow response to inspired CO 2 in the awake baboon (19).…”

Effects of carbon dioxide inhalation on cerebral blood flow and oxygen tissue level in spontaneously hypertensive rabbits.

“…26 ' 3031 ' 43 ' 47 These data also indicate that two kinds of CO 2 -CBF regulation exist, as was previously supposed. ' 45 It seems reasonable to assume that when neural regulation becomes damaged for various reasons, the direct effect of tissue Pco 2 on the vessel wall takes over.…”