J. Zhang et al., TIME-COURSE OF CHANGES IN ARTERIAL RELAXATION FOLLOWING SUBARACHNOID HEMORRHAGE IN DOGS, Neurological research, 18(3), 1996, pp. 227-232
This experiment determined ii the time course oi inhibition of arteria
l relaxation correlates with angiographic vasospasm following subarach
noid hemorrhage (SAH) in dogs. Twenty-two dogs underwent cerebral angi
ography followed by SAH by 2 injections of blood into the cisterna mag
na. Dogs had repeated angiography and were sacrificed 4 (n = 5), 7 (n
= 4), 10 (n = 4), 14 (n = 5), or 21 (n = 4) days later. Four dogs serv
ed as controls and underwent angiography only, followed by sacrifice.
The basilar arteries were removed and studied under isometric tension
to determine relaxations to acetylcholine and sodium nitroprusside. Th
ere was significant reduction in basilar artery diameter at each time
after SAH (day 4: -52% +/- 10%, day 7: -37% +/- 10%, day 10: -54% +/-
10%, day 14: -37% +/- 10%, and day 21: -26% +/- 18%, p < 0.05, analysi
s of variance), although there were no pairwise differences in the deg
ree of vasospasm over time. Relaxations to acetylcholine were signific
antly reduced at all times after SAH (p < 0.05, analysis of variance).
Relaxations to sodium nitroprusside were significantly reduced 7 days
after SAH. There was a significant linear correlation between increas
ing time after SAH and decreasing relaxation to acetylcholine. There w
as no correlation in univariate or multivariate analysis, between the
time after SAH, the degree of vasospasm and the relaxation to acetylch
oline or sodium nitroprusside. It is concluded that inhibition of arte
rial relaxation depends on the relaxant used and does not correlate wi
th vasospasm. The lack of correlation between angiographic vasospasm a
nd relaxation suggests that while the latter occurs after SAH, contrac
tile processes may be more important in the pathogenesis oi vasospasm.