Arterial CO2 tension is a powerful modulator of cerebral vascular calibre, CBF and ICP (12-15.) While the mechanisms are incompletely understood, CO2 relaxes pial arterioles by interactions between the endothelium, vascular smooth muscle, pericytes, adjacent neurons and glial cells. Studies supported that cerebral vessels are sensitive to changes in extracellular pH, rather than a direct response to CO2 or bicarbonate. In the limits of physiological PaCO2, 20-60 mmHg, the relationship between PaCO2 and CBF is linear. Therefore, increased PaCO2 results in vasodilation of cerebral vessels and this leads to increase CBF, increase CBV, decrease intracranial compliance and increase ICP. The reverse mechanism is also true for low CO2.
