Abstract
It remains unproven that the effect of hypercapnia on cerebral blood flow is entirely attributable to the associated change in ECF pH evoked by the rapid diffusion of carbon dioxide across the blood-brain barrier. This effect of hypercapnia on CBF can be blocked without any change in cerebral oxygen consumption by indomethacin, an inhibitor of prostaglandin synthesis (7). The CO2 response is also dependent on the resting level of cerebral oxygen consumption (4). We have suggested that an endogenous prostaglandin (or thromboxane) might provide a link between hypercapnia and cerebral vasodilatation. These considerations prompted us to quantify the effects of CO2 and ECF pH separately on a segment of the cerebrovascular tree, the middle cerebral artery (MCA), in vitro.
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References
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Pickard, J.D., Simeone, F.A., Vinall, P. (1976). H+, CO2, Prostaglandins and Cerebrovascular Smooth Muscle. In: Betz, E. (eds) Ionic Actions on Vascular Smooth Muscle. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-66427-4_21
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DOI: https://doi.org/10.1007/978-3-642-66427-4_21
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