Recently developed polarographic microelectrodes permit continuous, reliable monitoring of oxygen tension in brain tissue (PbrO2
). The aim of this study was to investigate the feasibility and utility of directly monitoring PbrO (2
) in cerebral tissue during changes in oxygenation or ventilation and during hemorrhagic shock and resuscitation. We also sought to develop a model in which treatment protocols could be evaluated using PbrO2
as an end point.
Licox Clark-type polarographic probes were inserted in the brain tissue of 16 swine to monitor PbrO2
. In eight swine, changes in PbrO2
were observed over a range of fractional concentrations of inspired O2
) as well as during periods of hyperventilation and hypoventilation. In eight other swine, PbrO2
was monitored during a graded hemorrhage of up to 70% estimated blood volume and during the resuscitation period.
was elevated to 100%, PbrO2
increased from a baseline of 15 +/- 2 mm Hg to 36 +/- 11 mm Hg. Hyperventilation while breathing 100% oxygen resulted in a 40% decrease in PbrO2
(p < 0.05), whereas hypoventilation increased PbrO2
to 88 mm Hg (p < 0.01). A graded hemorrhage to 50% estimated blood volume significantly reduced PbrO2
, mean arterial pressure, and intracranial pressure (p < 0.01). Continued hemorrhage to 70% estimated blood volume resulted in a PbrO (2
) of 2.9 +/- 1.5 mm Hg. After resuscitation, PbrO2
was significantly elevated, reaching 65 +/- 13 mm Hg (p < 0.01), whereas mean arterial pressure and cerebral perfusion pressure simply returned to baseline.
Directly measured PbrO2
was highly responsive to changes in FiO2
, ventilatory rate, and blood volume in this experimental model. In particular, hypoventilation significantly increased PbrO2
, whereas hyperventilation had the opposite effect. The postresuscitation increase in PbrO2
may reflect changes in both O2
delivery and O2
metabolism. These experiments set the stage for future investigations of a variety of resuscitation protocols in both normal and injured brain.