Abstract

To decipher the biophysical mechanism behind the fMRI-BOLD response to apnea and its dependence on the baseline cerebral blood flow and oxygenation, fMRI and laser Doppler flow (LDF) studies were carried out in anesthetized rats. Baseline cerebral blood flow (CBF) and PaO2 were modulated by ventilating with different gas mixtures namely, room air (21% O2), 100% O2, carbogen (95% O2+5% CO2), 2% CO2 in air or 5% CO2 in air, respectively. A decrease in BOLD signal intensity was observed after the onset of apnea with either room air, 2% CO2 or 5% CO2 ventilation. PaO2 and cerebral tissue PO2 decreased during apnea under these conditions. However, the apnea-induced BOLD signal intensity was unaffected with carbogen ventilation and increased with 100% O2 ventilation, during which PaO2 remained constant and cerebral tissue PO2 increased. When baseline CBF was high during hypercapnia, a faster decrease occurred in the apnea-induced BOLD signal. Apnea induced the largest increase in CBF of 85 +/- 25% when ventilated with 2% CO2 while a 44 +/- 8% increase was observed with room air. During the other ventilatory conditions, minimal or no significant change in CBF was observed during apnea. These results show a significant correlation between the BOLD signal change and tissue PO2 in response to apnea under different physiological conditions. Apnea-induced increase in CBF affects the magnitude of the BOLD signal response when PaO2 remains constant or changes minimally.

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