Cerebrovascular reactivity is severely affected by ischemia, and changes in
vascular responses have been reported after cortical spreading depression
and head trauma as well. Cortical depolarization (CD) occurs during ischemi
a, cortical spreading depression, and head trauma, but its effects on cereb
rovascular reactivity are unclear. We tested the hypothesis that CD induced
by KCI diminishes the vascular responsiveness to various vasodilatory stim
uli in piglets. Responses of pial arterioles were determined by changes in
vascular diameter by use of a closed cranial window and intravital microsco
py. Baseline arteriolar diameters were 105 +/- 3 mu m (mean +/- SEM, n = 27
). CD was elicited by topical administration of 1 mol/L KCl for 3 min. Vasc
ular responses were measured before and 1 h after CD. KCI elicited CD and c
onstricted arterioles by 54 +/- 4% (n = 27). N-methyl-D-aspartate induced d
ose-dependent vasodilation that was unaffected by CD; the percent changes w
ere 9 +/- 1 versus 8 +/- 1 (before and after CD) at 10(-5) mol/L, 19 +/- 2
versus 18 +/- 3 at 5 x 10-5 mol/L, and 29 +/- 2 versus 26 +/- 3 at 10(-4) m
ol/L (n = 9). Hypercapnic vasodilation was not diminished by CD; the percen
t changes were 15 +/- 2 I versus 16 +/- 4 at 5%, and 27 +/- 5 versus 27 +/-
6 at 10% inspired CO2 (n = 8), Aprikalim and forskolin caused dilation tha
t was also resistant to prior CD; the percent change values were 21 +/- 4 v
ersus, 18 +/- 3 and 16 +/- 2 versus 16 +/- 4 at 10(-6) mol/L, 36 +/- 5 vers
us 34 +/- 5 and 34 +/- 7 versus 37 +/- 7 at 10-5 mol/L (n = 8), respectivel
y. Finally, calcitonin gene-related peptide-induced vasodilation was unaffe
cted by CD; percent changes were 15 +/- 3 versus 16 +/- 2 at 10(-7) mol/L a
nd 26 +/- 4 versus 22 +/- 3 at 10(-4) mol/L (n = 8). The intact vascular re
sponses after CD suggest that this component is not responsible for decreas
ed cerebrovascular reactivity after ischemia, head trauma, or cortical spre
ading depression.