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

Abstract

The effects of acute and repeated exposures to 500 kPa O₂ on the distribution of cerebral blood flow$\left( {\dot Q_{CBF} } \right)$ 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$\left( {\dot Q_c } \right)$ and regional$\dot Q_{CBF}$ 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 andBP _a were higher andf _c was lower in group 2, while the acid-base chemistries were similar in the two groups. Total$\dot Q_{CBF}$ 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$\dot Q_c$ andf _c decreased, andBP _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$\dot Q_{CBF}$ and$\dot Q_{CBF}$ decreased in both groups, and the$\dot Q_{CBF}$ distribution was altered. Calculated O₂ supplies to different brain regions varied according to the$\dot Q_{CBF}$ changes, so that most regions sustained baseline O₂ delivery, although O₂ delivery to some regions may have been reduced. The decline of$\dot Q_{CBF}$ 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 O₂ on brain cells. In conclusion, repeated O₂ exposures induced heterogeneous and persistent changes in$\dot Q_{CBF}$, as well as a persistent increase in arterial pressure.