Nitric oxide promotes arteriolar dilation during cortical spreading depression in rabbits.

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Abstract
Pial arterioles transiently dilate during cortical spreading depression (CSD), although the mechanisms are unclear. We tested the hypothesis that increased production of nitric oxide (NO) promotes arteriolar dilation. Urethane-anesthetized rabbits were equipped with cranial windows, and the diameter (reported in micrometers) of a pial arteriole was determined via intravital microscopy. In each rabbit, a baseline CSD was elicited by microapplication of KCl onto the cortex, and resultant pial arteriolar dilation was measured. Either 100 mumol/L N omega-nitro-L-arginine methyl ester (L-NAME) or 50 mumol/L NG-nitro-L-arginine (L-NA), both competitive NO synthase inhibitors, was then applied to the brain surface. A CSD was elicited as before. The L-NAME and L-NA were then removed by artificial cerebrospinal fluid washes. An additional CSD was induced with KCl as before. Control CSD in the L-NAME group dilated pial arterioles; baseline diameter, 66 +/- 7 mm, with CSD = 106 +/- 8 mm (59% increase). After topically applied L-NAME, CSD dilated pial arterioles less: baseline diameter, 61 +/- 7 mm, with CSD = 77 +/- 6 mm (26% increase), P < .05 compared with control CSD diameter. Topical L-NA had similar effects on CSD: control CSD dilated pial arterioles 51%; after topical L-NA, only 14% (P < .05). After removal of L-NAME or L-NA, CSD-induced pial arteriolar dilation was similar to original control values. The reversible inhibition of CSD-induced pial arteriolar dilation by either L-NAME or L-NA suggests that NO contributes to arteriolar dilation observed with CSD.