The dura mater encephali is richly vascularized, possibly indicating a thermoregulatory function. We tested the hypotheses that the dural blood flow is thermoregulated and that the sensory neuropeptide calcitonin-gene-releated peptide (CGRP) is involved in this function.
For recording of dural blood flow, experiments were performed on barbiturate anesthetized rats. A parietal cranial window was trepanized in the skull and with a vortex thermode the dura mater was warmed and cooled. Blood flow in the middle meningeal artery was measured using laser Doppler flowmetry. The CGRP receptor antagonist CGRP8-37 and the local anaesthetic lidocaine were topically applied. For measurement of CGRP release from the dura mater, experiments were performed on isolated mice skull halves. CGRP release during different thermode-controlled temperatures was determined with an enzyme immunoassay.
During warming from 36°C to 45°C the dural blood flow raised slowly with a factor of 1,10 +/- 0,02 and reached a plateau. Immediately after cooling to 36°C the blood flow increased rapidly from the plateau forming a second short-lasting increase before it fell to the initial basal value. The effects were not significantly changed after application of CGRP8-37, whereas after lidocaine the cooling peak disappeared. Cooling did not increase the CGRP release from the dura mater.
The results, flow increases following heating as well as cooling, were unexpected. These responses may be part of a regulatory system that counteracts local temperature changes by blood flow increases. The cooling response involves probably a neuronal mechanism but CGRP seems not to play an important role.