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

The alterations in cerebral perfusion with graded hypercapnia were measured in the baboon using the intra-carotid 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 Pcoa. 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.