Local cerebral blood flow in spontaneously breathing rats subjected to graded isobaric hypoxia.

Local cerebral blood flow (l-CBF) was measured with an autoradiographic technique in spontaneously breathing rats exposed to air or gas mixtures of O2 and N2, giving inspired oxygen fractions (FiO2) ranging from 0.21 to 0.07. The arterial O2 tension (PaO2) changed from 10.9 +/- 0.3 (FiO2 0.21) to 3.9 kPa (FiO2 0.07) (82 +/- 2 to 29 mmHg). Hypoxia caused hyperventilation, and the arterial CO2 tension (PaCO2) fell from 5.21 +/- 0.05 kPa (FiO2 0.21) to 3.27 kPa (FiO2 0.07) (39.1 +/- 0.4 to 24.5 mmHg). The hyperventilatory response was markedly augmented when changing FiO2 from 0.13 to 0.11, causing a fall in PaCO2 of 0.75 kPa and a shift in arterial pH from 7.45 +/- 0.01 (FiO2 0.13) to 7.54 +/- 0.01 (FiO2 0.11). The l-CBF response to hypoxia was found to be biphasic for all the observed regions. At FiO2 0.13, l-CBF was measured about 75% above control but at FiO2 0.11, only 30% above control. A further reduction in FiO2 to 0.07 caused a marked increase in l-CBF, at least 240% of control; however, the applied CBF technique did not admit quantitation. These results suggest that the mechanisms controlling the cerebrovascular response to hypoxia and changes in arterial CO2 tensions are different. The results also indicate that hyperventilation might be harmful to the patient suffering from acute hypoxia.