Background: A decrease in brain temperature (T-brain) causes a decrease in the cerebral metabolic rate for oxygen (CMRO2) and provides potent neuroprotection against ischemic damage. In the present study, the effects of mild to moderate hypothermia on cerebral tissue oxygen tension (P-O2 brain), carbon dioxide tension (P-CO2 brain), and PH (PHbrain) were monitored during short episodes of global cerebral ischemia. Methods: After approval by the Animal Care and Use Committee, 10 New Zealand white rabbits were anesthetized (1% halothane in air) and mechanical ventilation was adjusted to maintain the arterial carbon dioxide tension at 35 mmHg (alpha-stat). A sensor to measure P-O2 brain, P-CO2 brain, PHbrain, and T-brain was inserted into the brain through a burr hole in the skull T-brain was adjusted to 38 degrees C, 34.4 degrees C, and 29.4 degrees C in a random sequence in each animal P-O2 brain, P(CO2)brain, and pH(brain) (all variables are reported at the actual T-brain) were recorded every 10 s during a 5-min baseline, 3 min of cerebral ischemia induced by inflation of a neck tourniquet, and 10 min of reperfusion at each level of T-brain. Analysis of variance and Dunnett's test were used for statistical analysis. Data are presented as means +/-SD. Results: During ischemia, P-O2 brain decreased from 56 +/- 3 to 33 +/- 2 mmHg at 38 degrees C, from 58 +/- 3 to 32 +/- 3 mmHg at 34.4 degrees C, and from 51 +/- 2 to 32 +/- 2 mmHg at 29.4 degrees C (p = NS). P-CO2 brain increased by 6.7 +/- 2 mmHg at 38 degrees C, by 5.1 +/- 1.4 mmHg at 34.4 degrees C, and by 2.3 +/- 0.8 mmHg at 29.4 degrees C. PHbrain, inversely followed the trend of P-CO2, brain. Conclusions: The attenuated increase in P-CO2 brain during hypothermic ischemia results from the reduced CMRO2. The similar decrease in P-O2 brain at all temperature levels indicates that despite the reduction in CMRO2, P-O2 brain is no better preserved during brief episodes of hypothermic ischemia than during normothermic ischemia.