Neurohypophyseal blood flow responses to hypoxia and hypercapnia were studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either decreasing O2 tension (hypoxic hypoxia, HH) or by increasing carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2 tension. In all animals HH and COH resulted in similar increases in total cerebral blood flow (239 and 300%, respectively). Regional cerebral blood flow showed a similar increase for all brain regions except the neurohypophysis (NH). The NH increased its blood flow with HH (approximately 320% of control) but was unchanged with COH (117% of control). The responsiveness of NH blood vessels was tested under conditions of hypercapnia (10% CO2) and HH with blood pressure controlled by concurrent hemorrhage. The response of NH vessels to altered arterial O2 tension occurs independently of blood pressure. Systemic [H+] or CO2 tension produce only small changes in NH blood flow. These data suggest that hypoxic and hypercapnic regulatory mechanisms for the NH are different from those of other brain regions. The precise mechanism by which the NH hypoxic response occurs remains unclear, but our data suggest an important role for systemic arterial O2 tension and chemoreceptors.
Relations of blood pressure and head injury to regional cerebral blood flow