Brain tissue oxygenation during hemorrhagic shock, resuscitation, and alterations in ventilation.
OBJECTIVE
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 PbrO2 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.


METHODS
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 (FiO2) 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.


RESULTS
When FiO2 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 PbrO2 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.


CONCLUSIONS
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.
Manley
G T
GT
School of Medicine, University of California San Francisco, Department of Neurological Surgery, San Francisco General Hospital, 94110, USA.
Pitts
L H
LH
Morabito
D
D
Doyle
C A
CA
Gibson
J
J
Gimbel
M
M
Hopf
H W
HW
Knudson
M M
MM
D000818:Animals; D001923:Brain Chemistry; D004195:Disease Models, Animal; D005240:Feasibility Studies; D006439:Hemodynamics; D018496:Hyperoxia / Q000150:complications / Q000378:metabolism*; D006985:Hyperventilation / Q000150:complications / Q000378:metabolism*; D007040:Hypoventilation / Q000150:complications / Q000378:metabolism*; D007427:Intracranial Pressure; D008297:Male; D008839:Microelectrodes; D008991:Monitoring, Physiologic / Q000295:instrumentation / Q000379:methods; D010100:Oxygen / Q000032:analysis*; D010101:Oxygen Consumption; D011048:Polarography / Q000295:instrumentation / Q000379:methods*; D015203:Reproducibility of Results; D012121:Respiration, Artificial / Q000379:methods; D012151:Resuscitation; D012771:Shock, Hemorrhagic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D013552:Swine
D010100:Oxygen