| Literature DB >> 8983913 |
Abstract
Hyperbaric oxygen at pressures of 300 to 500 kPa has been shown to induce changed distribution of cerebral blood flow (QCBF) in rats, in places reducing the supply of the supplementary O2. Thus, in the present study, the effect of hyperoxia at 101 (group 1, n = 9) and 150 (group 2, n = 9) kPa O2 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 (fc), breathing frequency (fb), cardiac output (Qc), arterial acid-base chemistry and glucose, as well as QCBF distribution (rQCBF) were similar in the two groups of animals. During O2 exposure, the acid-base chemistry remained unchanged. The haemoglobin decreased in group 2, but remained unchanged in group 1. The fc decreased rapidly in both groups during the change in gas composition, after which fc remained constant both in group 1 and in group 2, for whom pressure was increased. The Qc and fb decreased and BPs increased similarly in the two groups. Total QCBF and rQCBF decreased to the same extent in both groups, and the rQCBF changes were equally scattered. In group 1, breathing of pure O2 did not increase the O2 supply to any cerebral region except to the thalamus and colliculi after 60 min, whereas the O2 supply to the hypothalamus decreased and remained low. In group 2, the O2 supply was unchanged compared to the control period in all regions. These findings agree with previous observations during exposures to higher O2 pressures. In air after O2 exposure the acid-base chemistry remained normal. The fc and fb increased to higher levels than during the control period. The BPs remained high. The brain blood flows were increased, inducing elevated O2 supply to several brain regions compared to the control period. In conclusion, O2 supply to the central nervous system was found to be in the main unchanged during breathing of O2 at 101 kPa and 150 kPa.Entities:
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Year: 1995 PMID: 8983913 DOI: 10.1007/bf00238548
Source DB: PubMed Journal: Eur J Appl Physiol Occup Physiol ISSN: 0301-5548