Rat Brain Glucose and Energy Metabolites: Effect of +Gz(Head-to-Foot Inertial Load) Exposure in a Small Animal Centrifuge

A unique small animal centrifuge with on-line physiological monitoring and brain tissue collection (in < 1 s) capability was used to investigate the effect of increasing + G z levels, exposure duration, number of exposures, and time course of metabolic changes in the rat brain. To determine the + G z tolerance, rats were exposed to +7.5 to 25 G z (30 s each) and EEG was monitored. G-induced loss of consciousness ( G-LOC) defined as isoelectric EEG (I-EEG) occurred only at +22.5 and 25 G z within 14.5 ± 3 s. To study the effect of increasing + G z levels on metabolism, rats were exposed to either 0.5 (control) or +7.5 to 25 G z (30 s each), and brains were collected 1 min postcentrifugation by freeze fixation. A significant increase in lactate (≥ + 7.5 G z ) and a decrease in glucose, creatine phosphate (Cr-P), and ATP levels were observed at + 15 G z and higher. The effect of exposure duration was investigated by exposing the rats to + 22.5 G z for 15–60 s. Brain lactate levels increased sixfold while glucose decreased (75%) following the 60-s exposure. The level of Cr-P and ATP decreased significantly after the 15- and 30-s exposures with no further changes at longer + G z exposures. For time course studies, brains were collected both during (5–35 s) and after (1–15 min) a +25 G z exposure. A significant decrease in Cr-P occurred within 5 s, but changes in glucose, ATP, and lactate required 15 s. All metabolites returned to control levels within 3 min, except lactate and adenosine, which required 15 min. Exposure of rats to either one, three, or five runs at +22.5 G z (30 s each) resulted in an increase in lactate (ninefold) and a decrease in glucose (87%). Both Cr-P and ATP decreased after one exposure with no further change after three and five exposures. These results show that + G z exposures of short duration cause significant transient metabolic alterations consistent with global cerebral ischemia. We propose that G-LOC (I-EEG) may be an acute response of the CNS to high + G z -imposed ischemic stress. G-LOC would reduce the overall brain energy demand and thus reduce anaerobic glycolysis and lactate production.