Effects of blood pressure change upon brain-stem pO2 in rabbits with surgically removed baroreceptor nerve. Possible mechanisms for vertigo due to autonomic nerve dysfunction.

The effect of denervation of carotid sinus nerve (CSD) on the brain-stem tissue pO2 tension was studied in the awake rabbit. Tissue pO2 around the vestibular nuclei was measured in two groups of rabbits, normal and CSD, under two experimental conditions, viz. blood pressure (BP) modulation and tilt stimulation. BP was either depressed by hemorrhage (up to 50 mmHg) or elevated by intravenous injection of phenylephrine (up to 160 mmHg). In the normal rabbit, tissue pO2 showed minimum change during BP modulation (ranging between 70 and 160 mmHg. In contrast, CSD surgery resulted in the failure to maintain pO2 at a constant level when BP was elevated. However, tissue pO2 did not change when BP decreased. Head-up tilt stimulation (up to 40 degrees) also induced a transient decrease in BP and pO2 in the CSD rabbit; however, these were maintained at a constant level in the normal rabbit. These conditions were assumed to be due to the decrease in autoregulation of cerebral blood flow (CBF), which resulted in CSD. In these experiments, tissue pO2 recovered first, even when BP still remained low. Therefore, it can be proposed that the carotid baroreceptor reflex works for CBF autoregulation of brain stem primarily during an early phase of BP change. Therefore a disturbed carotid sinus reflex, as shown in the present experiment, may be a possible explanation for the mechanism of stress-related vertigo and/or orthostatic vertigo.