• G W Bergø and I Tyssebotn.
• Department of Physiology, University of Bergen, Norway.
• J. Appl. Physiol. 1995 Jun 1; 78 (6): 2100-8.

AbstractCerebral blood flow (CBF), systemic hemodynamics, and arterial blood gases were measured during control conditions and during and after exposure to either 300 kPa O2 (group 1) or 300 kPa O2 with 2 kPa CO2 (group 2) in awake rats. The respiratory frequency fell with no change of arterial PCO2 (PaCO2) in group 1, but in group 2, respiratory frequency and PaCO2 increased linearly. The cardiac output (CO) and heart rate (HR) fell and systolic arterial pressure (SAP) rose independent of PACO2. O2 breathing caused CBF to fall by 30% in group 1, whereas CBF rose linearly with the PaCO2 increase and pH decline in group 2. Regional CBF (rCBF) fell in group 1, whereas rCBF rose gradually in all regions in group 2, but the responses varied similarly in both groups. Regional brain O2 supply was unaltered in most areas. However, the O2 supply was possibly reduced in the brain stem in group 1 but markedly increased in group 2. After decompression, HR and SAP were high, whereas CO returned to its control value. CBF and all rCBF levels remained markedly elevated in group 2. In group 1, CBF returned to control levels. By contrast, rCBF and O2 delivery to brain stem regions remained subnormal. In conclusion, the O2-induced changes in HR, CO, and SAP were not influenced by hypercapnia. CBF and rCBF fell despite unaltered PaCO2, whereas hypercapnia prevented these declines. An uneven effect of O2 was observed on rCBF, most pronounced in brain stem regions, independent of the PaCO2. There was a prolonged suppression of O2 supply to brain stem regions both during and after the exposure to O2 in the absence of CO2.

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