Cerebral circulatory responses to arterial hypoxia in normal and chemodenervated dogs.

Abstract

Listen

Translate article

SUMMARY Cerebral hemodynamic responses to arterial hypoxia were studied in 13 normal and 9 chemodenervated anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18.0 vol%) to 14.0, 8.0, and 4.0 vol%, respectively, by either decreasing arterial Po2 (hypoxic hypoxia) or increasing carboxyhemoglobin saturation (CO hypoxia) at normal Po2. Both hypoxic hypoxia and CO hypoxia at each value of the lowered arterial O2 content resulted in progressive significant increases in cerebral blood flow (134, 169, 276, and 146, 206, 244% of control, respectively). Before chemoreceptor denervation, arterial blood pressure increased with hypoxic hypoxia but decreased with CO hypoxia. After chemodenervation, hypoxic hypoxia and CO hypoxia at each value of lowered arterial O2 content resulted in similar significant increases in cerebral blood flow. These increases were not significantly different from those observed prior to chemodenervation. After chemodenervation, hypoxic hypoxia and CO hypoxia both resulted in similar decreases in arterial blood pressure and cerebral vascular resistance, whereas, before chemodenervation, cerebral vascular resistance decreased more with CO hypoxia than with hypoxic hypoxia. These data show that cerebral vasodilation induced by both forms of hypoxia in chemodenervated dogs resembles that in animals with CO hypoxia and intact chemoreceptors in which Pao2 is high and the carotid chemoreceptors may not be activated. We also have shown that the transient responses to both types of hypoxia are not altered by carotid chemodenervation, and conclude that the carotid chemoreceptors do not play a role in the mechanism by which cerebral blood flow increases during decreased blood O2 content. IN THE PAST several years, there has been renewed interest in the possible role of the autonomic nervous system in the regulation of cerebral blood flow. Despite much evidence supporting an autonomic nerve supply to parts of the cerebral vasculature, the functional significance of these nerves remains uncertain. Neural regulatory mechanisms for the cerebral circulation have been assumed to be negligible or nonexistent' because of the failure of autonomic stimulation and denervation to affect cerebral blood flow significantly. The effect of the sympathetic nervous system on cerebral blood flow remains especially controversial. Many investigators have failed to show any significant effects of sympathetic stimulation on cerebral blood flow, 2 " 4 whereas others using similar tech