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 distribution of cerebral blood flow (Q(CBF)) and systemic haemodynamics were 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 pressure (BPa), and heart rate (f(c)) were measured continuously from implanted 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 all the animals. The baseline measurements in air of BPs and BPa were higher and f(c) was lower in group 2, while the acid-base chemistries were 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 colliculi, hippocampus, hypothalamus, and most cerebral cortical regions were higher, but lower to pens and medulla oblongata. During O-2 exposure Q(c) and f(c) decreased, and BPa, BPs, and peripheral vascular resistance 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 could have been elevated, thereby potentiating the toxic effects of O-2 on brain cells. In conclusion, repeated O-2 exposures induced heterogeneous and persistent changes in Q(CBF), as well as a persistent increase in arterial pressure.