CEREBRAL BLOOD-FLOW DISTRIBUTION AND SYSTEMIC HEMODYNAMIC-CHANGES AFTER REPEATED HYPERBARIC-OXYGEN EXPOSURES IN RATS

The effects of acute and repeated exposures to 500 kPa O-2 on the dist ribution of cerebral blood flow (Q(CBF)) and systemic haemodynamics we re assessed in awake rats. After habituation, the control rats (group 1, n = 7) were restrained for 1 h daily for 8 days in air at 101 kPa, while the test rats (group 2, n = 8) were exposed to 500 kPa O-2 for 1 h daily for 8 consecutive days. During a final exposure, both groups were exposed to 500 kPa O-2. Systolic (BPs) and mean arterial blood pr essure (BPa), and heart rate (f(c)) were measured continuously from im planted arterial catheters; while cardiac output (Q(c)) and regional Q (CBF) (rQ(CBF)) were measured by the microsphere method in air before the O-2 exposure, and after both 5 min and 60 min at 500 kPa O-2 in al l the animals. The baseline measurements in air of BPs and BPa were hi gher and f(c) was lower in group 2, while the acid-base chemistries we re similar in the two groups. Total Q(CBF) was similar in both groups. However in group 2, blood flows and calculated O-2 supplies to collic uli, hippocampus, hypothalamus, and most cerebral cortical regions wer e higher, but lower to pens and medulla oblongata. During O-2 exposure Q(c) and f(c) decreased, and BPa, BPs, and peripheral vascular resist ance increased in all the rats. Arterial partial pressure of CO2 and [ HCO3-] decreased in group 1, but remained at baseline levels in group 2. Total Q(CBF) and rQ(CBF) decreased in both groups, and the rQ(CBF), distribution was altered. Calculated O-2 supplies to different brain regions varied according to the rQ(CBF) changes, so that most regions sustained baseline O-2 delivery, although O-2 delivery to some regions may have been reduced. The decline of rQ(CBF) also indicated reduced removal of waste from the brain, so that CO2 tension and temperature c ould have been elevated, thereby potentiating the toxic effects of O-2 on brain cells. In conclusion, repeated O-2 exposures induced heterog eneous and persistent changes in Q(CBF), as well as a persistent incre ase in arterial pressure.