The Role of the Carotid Body in Acclimatization to Hypoxia

Abstract

Ventilatory acclimatization to hypoxia (VAH) is the time-dependent increasing hyperventilation that occurs during prolonged exposure to hypoxia. The carotid chemoreceptors are responsible for the acute ventilatory response to hypoxia and they are recognized as critical to at least the initiation of VAH (Forster et al., 1976, 1981: Smith et al., 1984). Beyond the initial acute hypoxic hyperventilation the mechanism of VAH has been controversial. Several mechanisms associated with brain hypoxia have been proposed previously, e.g., acidification of cerebral interstitial fluid in the environment of the central chemoreceptors (Fencl et al., 1979), changes in brain monoamine metablolism (Olson et al., 1983) and suprapontine facilitation of respiratory activity (Tenney and Ou, 1977). It is clear that brain hypoxia alone cannot initiate VAH since it does not proceed normally in the absence of the carotid chemoreceptors (Forster et al., 1976, 1981: Smith et al., 1984). However, it remains unclear as to the role brain hypoxia and acid-base changes play in VAH. Similarly the role of the peripheral chemoreceptors remains unclear. Therefore, we asked the following questions: l) Is brain hypoxia a necessary component of the mechanism of VAH? 2) Does hypocapnic alkalosis play a critical role in VAH? and 3) Can VAH be induced by different modes of carotid body (CB) stimuli?