Cerebral hemodynamics during cortical spreading depression in rabbits

Abstract

Effects of a sibgle cortical spreading depression (CSD), elicited by KCl microinjection, on diameter of pial arterioles and venules in the parieto-occipital cortex were examined in urethane-anesthetized adult rabbits using a closed cranial window. The velocity of CSD propagation was2.7±0.1mm/min (mean±S.E.M.). All arterioles (n=39) except for those in the retrosplenial region (n=6) increased their diameter significantly during CSD. The arteriolar dilation lasted for1.5±0.1min. Location of dilating arteriole and propagating CSD showed that they were always closely associated temporally. As a percentage change, diameters of smaller arterioles significantly increased (from60 ± 1to103 ± μm, 71%, n = 12) more than those of larger ones (from82 ± 2to129 ± 3 μm, 57%, n = 27). While venules with initial diameter of85 ± 4 μm(n = 5) did not dilate, those with initial diameter of49 ± 3 μm increased to57 ± 3 μm(16%, n = 8) for1.4 ± 0.2 min during CSD. The majority of the dilated venules started to increase their diameter after nearby arterioles had dilated maximally. Pial arterioles, which dilated during ipsilateral CSD, decreased their diameter significantly from78 ± 2to72 ± 3 μm(8%, n = 11) during contralateral CSD for13.8 ± 3.6min with similar onset latencies as those observed for the dilation. Indomethacin pretreatment significantly enhanced arteriolar dilation during CSD (from73 ± 4to138 ± 6 μm, 89%, n =4). The results indicate that pial arteriolar dilation observed during CSD is an active response, and probably caused by an excitatory rather than inhibitory effect accompanying CSD, and that prostanoids may play an important modulatory role.