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 g ases were measured during control conditions and during and after expo sure to either 300 kPa O-2 (group 1) or 300 kPa O-2 with 2 kPa CO2 (gr oup 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 frequ ency and Pa-CO2 increased linearly. The cardiac output (CO) and heart rate (HR) fell and systolic arterial pressure (SAP) rose independent o f 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 al l regions in group 2, but the responses varied similarly in both group s. 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 mark edly increased in group 2. After decompression, HR and SAP were high, whereas CO returned to its control value. CBF and all rCBF levels rema ined markedly elevated in group 2. In group 1, CBF returned to control levels. By contrast, rCBF and O-2 delivery to brain stem regions rema ined subnormal. In conclusion, the O-2-induced changes in HR, CO, and SAP were not influenced by hypercapnia. CBF and rCBF fell despite unal tered Pa-CO2, whereas hypercapnia prevented these declines. An uneven effect of O-2 was observed on rCBF, most pronounced in brain stem regi ons, 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.