Cerebrospinal fluid pressures during hypercapnia and hypoxia in dogs

Abstract

Cerebrospinal fluid pressure (CSFP) in the cisterna magna, intra-aortic and intrathoracic venous pressures were measured during apneic oxygenation (diffusion respiration) in dogs under light pentobarbital-succinylcholine anesthesia. CSFP doubled in 2 minutes and reached a peak 375% above control in 10 minutes. During this time there were no consistent changes in arterial or venous pressures. Dogs ventilated with 5, 10 and 15% CO2 showed a similar pattern. Cerebral vasodilatation caused by CO2 is the probable mechanism in both groups. A sustained elevation of CSFP was observed throughout CO2 administration for as long as 90 minutes. In all cases there was a prompt return to control levels on termination of the hypercapnia. Controlled ventilation with 8% O2 caused an average 84% rise in CSFP, with a plateau occurring after 4–5 minutes. This was accompanied by marked increases in arterial and venous pressures. Cerebral vasodilatation probably occurs here also. During 90 seconds of asphyxia the sharpest increase (175%) in CSFP occurred. This was accompanied by marked increases in arterial and venous pressures, and represents the effect of hypoxia and hypercapnia combined.