Cerebral blood flow distribution and systemic haemodynamic changes after repeated hyperbaric oxygen exposures in rats

The effects of acute and repeated exposures to 500 kPa O₂ on the distribution of cerebral blood flow {Mathematical expression} 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 O₂ for 1 h daily for 8 consecutive days. During a final exposure, both groups were exposed to 500 kPa O₂. Systolic (BP_s) and mean arterial blood pressure (BP_a), and heart rate (f_c) were measured continuously from implanted arterial catheters; while cardiac output {Mathematical expression} and regional {Mathematical expression} were measured by the microsphere method in air before the O₂ exposure, and after both 5 min and 60 min at 500 kPa O₂ in all the animals. The baseline measurements in air of BP_s and BP_a were higher and f_c was lower in group 2, while the acid-base chemistries were similar in the two groups. Total {Mathematical expression} was similar in both groups. However in group 2, blood flows and calculated O₂ supplies to colliculi, hippocampus, hypothalamus, and most cerebral cortical regions were higher, but lower to pons and medulla oblongata. During O₂ exposure {Mathematical expression} and f_c decreased, and BP_a, BP_s, 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 {Mathematical expression} and {Mathematical expression} decreased in both groups, and the {Mathematical expression} distribution was altered. Calculated O₂ supplies to different brain regions varied according to the {Mathematical expression} changes, so that most regions sustained baseline O₂ delivery, although O₂ delivery to some regions may have been reduced. The decline of {Mathematical expression} 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 O₂ on brain cells. In conclusion, repeated O₂ exposures induced heterogeneous and persistent changes in {Mathematical expression}, as well as a persistent increase in arterial pressure.