Effects on brain tissue-oxygen level during acceleration stress in anesthetized rats

Abstract

High sustained +Gz stress has been known to provoke G induced loss of consciousness and central nervous system insults. Direct recording of tissue PO₂ in the brain during +Gz exposure has not yet been reported. The purpose of this study is to evaluate effects of +Gz stress in the brain PO₂. Anesthetized male SD rats were exposed to +3Gz by a centrifuge with an anti-G suit. Arterial pressure level of the brainstem (APLB), central venous pressure, heart rate and PO₂ of the brain were measured. Cortical and hippocampal PO₂ were simultaneously measured by a PO₂ monitor with the polarographic oxygen electrodes. A decrease in APLB was observed twice: during the phase of increasing +Gz and the phase of decreasing +Gz. At these lowest points, cortical and hippocampal PO₂ were also decreased significantly (first: 83.0 ± 2.4% and 68.8±4.4%; second: 81.0 ± 1.6% and 71.7 ± 6.7%; vs. control). APLB was restored to the control level just after the +Gz exposure was stopped. However, cortical PO₂ was not restored to the control level over 5 minutes after the +Gz stop, although hippocampal PO₂ was restored until 1 minute. +Gz induced hypotension involved a decrease in brain-tissue oxygen concentration. However, the time course of the PO₂ changes during the +Gz exposure were different between cortex and hippocampus. This result may describe that the +Gz effect on the brain oxygen concentration is different dependently on the brain areas. [J Physiol Sci. 2008;58 Suppl:S110]