CEREBRAL HEMODYNAMICS DURING CORTICAL SPREADING DEPRESSION IN RABBITS

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 was 2.7±0.1 mm/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 for 1.5±0.1 min. 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 (from 60 ± 1 to 103 ± μm, 71%, n = 12) more than those of larger ones (from 82 ± 2 to 129 ± 3 μm, 57%, n = 27). While venules with initial diameter of 85 ± 4 μm (n = 5) did not dilate, those with initial diameter of 49 ± 3 μm increased to 57 ± 3 μm (16%, n = 8) for 1.4 ± 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 from 78 ± 2 to 72 ± 3 μm (8%, n = 11) during contralateral CSD for 13.8 ± 3.6 min with similar onset latencies as those observed for the dilation. Indomethacin pretreatment significantly enhanced arteriolar dilation during CSD (from 73 ± 4 to 138 ± 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. © 1990.