Cerebrovascular response to hypoxia in baroreceptor- and chemoreceptor-denervated dogs

R. J. Traystman, R. S. Fitzgerald

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


Cerebral hemodynamic responses to arterial hypoxemia were studied in anesthetized paralyzed dogs that were or that had undergone carotid baroreceptor denervation, carotid chemoreceptor denervation, vagotomy, or both vagotomy and carotid sinus nerve section. Arterial O2 content was lowered from control (19.0 vol%) to 9.6 vol% by either decreasing arterial O2 tension [hypoxic hypoxemia (HH)] or increasing carboxyhemoglobin saturation [carbon-monoxide hypoxemia (COH)] at normal O2 tension. In intact animals (composite control values from all groups) HH and COH resulted in similar increases in cerebral blood flow (to 205 and 197% of control, respectively). Cerebral vascular resistance decreased more with COH than with HH (to 42 vs 60% of control). The response from carotid baroreceptor-denervated animals and from vagotomized animals did not differ from that of the intact animals. After carotid chemoreceptor denervation and combined carotid sinus nerve section and vagotomy, both HH and COH increased cerebral blood flow to 194% of control (same increase as in intact animals, carotid baroreceptor-denervated animals and vagotomized animals) and produced equal reductions in cerebral vascular resistance (to 34% of control). These data show that the carotid and aortic chemoreceptors are not necessary for the increase in cerebral blood flow provoked by hypoxemia and that this response is not modified by the carotid and aortic baroreceptors.

Original languageEnglish (US)
Pages (from-to)724-731
Number of pages8
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5
StatePublished - 1981

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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