Hanley D F, Wilson D A, Traystman R J
Am J Physiol. 1986 Jan;250(1 Pt 2):H7-15. doi: 10.1152/ajpheart.1986.250.1.H7.
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.
在戊巴比妥麻醉、麻痹的犬类中研究了神经垂体对缺氧和高碳酸血症的血流反应。通过在正常氧分压下降低氧张力（低氧性缺氧，HH）或增加碳氧血红蛋白饱和度（一氧化碳缺氧，COH），使动脉血氧含量从对照值（18±2容积%）降至8±1容积%。在所有动物中，HH和COH均导致全脑血流量相似增加（分别为239%和300%）。除神经垂体（NH）外，所有脑区的局部脑血流量均有相似增加。NH的血流量在HH时增加（约为对照值的320%），但在COH时无变化（为对照值的117%）。在高碳酸血症（10%二氧化碳）和HH条件下，通过同时出血控制血压来测试NH血管的反应性。NH血管对动脉血氧张力改变的反应独立于血压。全身[H⁺]或二氧化碳张力仅使NH血流量产生微小变化。这些数据表明，NH的缺氧和高碳酸血症调节机制与其他脑区不同。NH缺氧反应发生的确切机制尚不清楚，但我们的数据表明全身动脉血氧张力和化学感受器起重要作用。
