RAT-BRAIN GLUCOSE AND ENERGY METABOLITES - EFFECT OF -TO-FOOT INERTIAL LOAD) EXPOSURE IN A SMALL ANIMAL CENTRIFUGE(G(Z) (HEAD)

A unique small animal centrifuge with on-line physiological monitoring and brain tissue collection (in < 1 s) capability was used to investi gate 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 df 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 postcentr ifugation by freeze fixation. A significant increase in lactate (great er than or equal to + 7.5 G(z)) and a decrease in glucose, creatine ph osphate (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 six-fold wh ile 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 st udies, 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 metab olites returned to control levels within 3 min, except lactate and ade nosine, 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 lac tate (ninefold) and a decrease in glucose (87%). Both Cr-P and ATP dec reased 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 glob al cerebral ischemia. We propose that G-LOC (I-EEG) may be an acute re sponse of the CNS to high + G(z)-imposed ischemic stress. G-LOC would reduce the overall brain energy demand and thus reduce anaerobic glyco lysis and lactate production.