CEREBRAL BLOOD-FLOW AND SYSTEMIC HEMODYNAMICS DURING EXPOSURE TO 2-KPA CO2 TO 300-KPA O-2 IN RATS

Cerebral blood flow (CBF), systemic hemodynamics, and arterial blood gases were measured during control conditions and during and after exposure to either 300 kPa O-2 (group 1) or 300 kPa O-2 with 2 kPa CO2 (group 2) in awake rats. The respiratory frequency fell with no change of arterial P-CO2 (Pa-CO2) in group 1, but in group 2, respiratory frequency and Pa-CO2 increased linearly. The cardiac output (CO) and heart rate (HR) fell and systolic arterial pressure (SAP) rose independent of Pa-CO2. O-2 breathing caused CBF to fall by 30% in group 1, whereas CBF rose linearly with the Pa-CO2 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 O-2 supply was unaltered in most areas. However, the O-2 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 O-2 delivery to brain stem regions remained subnormal. In conclusion, the O-2-induced changes in HR, CO, and SAP were not influenced by hypercapnia. CBF and rCBF fell despite unaltered Pa-CO2, whereas hypercapnia prevented these declines. An uneven effect of O-2 was observed on rCBF, most pronounced in brain stem regions, independent of the Pa-CO2. There was a prolonged suppression of O-2 supply to brain stem regions both during and after the exposure to O-2 in the absence of CO2.