Cerebrospinal fluid alkalosis during high-altitude sojourn in unanesthetized ponies

Abstract

Unanesthetized adult female ponies were studied near sea level (250 m) and during sojourns to 3400 m (N = 6) and 4300 m (N = 7) altitude. The pH, P CO 2 and P O 2 , of arterial blood and pH and P CO 2 , of cerebrospinal fluid (CSF) were measured under conditions of acute (1 hr) and chronic (1–45 days) hypoxia. Cerebrospinal fluid was sampled from the cisterna magna of the awake pony and arterial blood withdrawn from an indwelling arterial catheter. In both groups of animals, Pa CO 2 , decreased slightly after 1 hr of hypoxia ( ΔPa CO 2 = −0.6 mm Hg at 3400 m; −3.9 mm Hg at 4300 m), decreased further after 1–5 days at high altitude ( ΔPa CO 2 = −7.2 mm Hg at 3400 m: −12.3 mm Hg at 4300 m) and then increased significantly after 6 days of chronic hypoxia ( ΔPa CO 2 = +4.1 mm Hg at 3400 m; +4.7 mm Hg at 4300 m). Although Pa O 2 , decreased markedly during acute hypoxia, subsequent changes in Pa CO 2 at high altitude did not alter Pa O 2 from that observed during acute hypoxia ( Pa O 2 = 52 mm Hg at 3400 m; 41 mm Hg at 4300 m). The pH of CSF increased during acute hypoxia (ΔpH = +0.013 unit at 3400 m; +0.033 unit at 4300 m) and became more alkaline after 1–2 days at high altitude (ΔpH = +0.031 unit at 3400 m; +0.064 unit at 4300 m). At 4300 m, CSF pH remained alkaline to control values throughout sojourn. Under these conditions of chronic hypocapnic hypoxia, CSF pH was imperfectly regulated and regulated in a magnitude equal to (3400 m) or less than (4300 m) arterial blood. Furthermore, the similarity of relative changes in CSF [HCO 3] and arterial [HCO 3] during chronic hypoxia may indicate a passive regulation of CSF [HCO 3] rather than local ‘CSF-specific’ mechanisms as previously proposed.