• C O Borel, J E Backofen, R C Koehler, M D Jones, and R J Traystman.
• Department of Anesthesiology/Critical Care Medicine, Eudowood Neonatal Pulmonary Division, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
• Am. J. Physiol. 1987 Dec 1; 253 (6 Pt 2): H1342-8.

AbstractWe tested the hypothesis that hypoxic hypoxia interferes with cerebral blood flow (CBF) autoregulation when intracranial pressure (ICP) is elevated in pentobarbital-anesthetized lambs (3 to 9 days old). Cerebral perfusion pressure (CPP) was lowered stepwise from 73 to 23 mmHg in eight normoxic lambs and from 65 to 31 mmHg in eight other hypoxic lambs by ventricular infusion of artificial cerebrospinal fluid. In normoxic lambs, CBF measured by microspheres was not significantly changed over this range of CPP. In animals made hypoxic [arterial O2 tension (PaO2) of 28 Torr; 47% arterial O2 saturation], base-line CBF was twice that of normoxic lambs. CBF was unchanged as CPP was reduced to 31 mmHg. Lower levels of CPP were not attained because a pressor response occurred with further elevations of ICP. No regional decrements in blood flow to cortical arterial watershed areas or to more caudal regions, such as cerebellum, brain stem, or thalamus, were detected with elevated ICP. Cerebral O2 uptake was similar in both groups and did not decrease when CPP was reduced. These results demonstrate that normoxic lambs have a considerable capacity for effective autoregulation of CBF when ICP is elevated. Moreover, cerebral vasodilation in response to a level of hypoxia approximating that normally seen prenatally does not abolish CBF autoregulation when ICP is elevated during the first postnatal week.

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