Hyperbaric oxygen at pressures of 300 to 500 kPa has been shown to induce changed distribution of cerebral blood flow (Q(CBF)) in rats, in places reducing the supply of the supplementary O-2. Thus, in the present study, the effect of hyperoxia at 101 (group 1, n = 9) and 150 (group 2, n = 9) kPa O-2 on cerebral blood flow distribution and central haemodynamics was tested in conscious, habituated rats. During the control period the systolic arterial pressure (BPs), heart rate (f(c)), breathing frequency (f(b)), cardiac output (Q(c)), arterial acid-base chemistry and glucose, as well as Q(CBF) distribution (rQ(CBF)) were similar in the two groups of animals. During O-2 exposure, the acid-base chemistry remained unchanged. The haemoglobin decreased in group 2, but remained unchanged in group 1. The f(c) decreased rapidly in both groups during the change in gas composition, after which f(c) remained constant both in group 1 and in group 2, for whom pressure was increased. The Q(c) and f(b) decreased and BPs increased similarly in the two groups. Total Q(CBF) and Q(CBF) decreased to the same extent in both groups, and the rQ(CBF) changes were equally scattered. In group 1, breathing of pure O-2 did not increase the O-2 supply to any cerebral region except to the thalamus and colliculi after 60 min, whereas the O-2 supply to the hypothalamus decreased and remained low. In group 2, the O-2 supply was unchanged compared to the control period in all regions. These findings agree with previous observations during exposures to higher O-2 pressures. In air after O-2 exposure the acid-base chemistry remained normal. The f(c) and f(b) increased to higher levels than during the control period. The BPs remained high. The brain blood flows were increased, inducing elevated O-2 supply to several brain regions compared to the control period. In conclusion, O-2 supply to the central nervous system was found to be in the main unchanged during breathing of O-2 at 101 kPa and 150 kPa.
