Stroke, Vol 25, 2463-2470, Copyright © 1994 by American Heart Association
DM Colonna, W Meng, DD Deal and DW Busija
BACKGROUND AND PURPOSE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
ARTICLES
Nitric oxide promotes arteriolar dilation during cortical spreading depression in rabbits
Department of Anesthesia, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1009.
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