Effect of exposure to oxygen at 101 and 150 kPa on the cerebral circulation and oxygen supply in conscious rats

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.

Mild and Moderate Hypothermia (α-Stat) Do Not Impair the Coupling Between Local Cerebral Blood Flow and Metabolism in Rats

“…Experimental and human studies demonstrated that hyperoxia may slightly reduce CBF, especially under hyperbaric conditions. 36,37 However, PaO 2 values observed during hyperbaric oxygenation are markedly higher than those in the present investigation (PaO 2 Ϸ200 mm Hg). James et al 38 observed that increasing PaO 2 above the normal range (up to 450 mm Hg) does not significantly influence gray and white matter blood flow.…”

Treatment of Cerebral Radionecrosis by Hyperbaric Oxygen Therapy

“…Total CBF is decreased between 20 and 30%, while the oxygen supply is still maintained [10][11][12]. However, experimental data show that changes of CBF caused by HBO are dependent on the region, and also areas of increased CBF were found [13].…”

Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide

“…The present data demonstrate that normal lung function and respiratory regulation were preserved during this O 2 pressure, which is a common treatment pressure for humans. The respiratory balance has also been reported to be normal in normoxic hyperbaric exposures of up to 4.1 MPa (Furset et al 1989;Risberg et al 1990;Bergù and Tyssebotn 1995b). Conversely, hyperventilation occurred during O 2 exposures to pressure that exceeds those used for clinical treatment; 350 kPa O 2 in man (Lambertsen 1978) and 500 kPa O 2 in rats (Bergù et al 1988;Bergù and Tyssebotn 1992a).…”

“…The unchanged EDP and SV eliminate FrankStarting mechanisms as an explanation for the increase in LVP and cardiac contractility. Thus, the augmented hemodynamic parameters may be due to the combined eects of the ambient pressure increase per se (Ask and Tyssebotn 1988;Stuhr et al 1989), an increase in breathing gas density (Bergù and Tyssebotn 1992c;Risberg et al 1995), and the O 2 pressure increase (Bergù and Tyssebotn 1995b;Risberg et al 1995). Of these factors, the increase in O 2 pressure has been shown to be most potent since a pressure increase of only 10 kPa O 2 reduces f c and increases cardiac contractility (Risberg et al 1995), whereas normoxic ambient pressures up to 7 MPa (Aanderud et al 1985;Stuhr et al 1989) did not in¯uence the f c , but increased contractility (Ask and Tyssebotn 1988;Stuhr et al 1989).…”