T. Mori et al., SUPEROXIDE ANIONS IN THE PATHOGENESIS OF TALC-INDUCED CEREBRAL VASOCONTRACTION, Neuropathology and applied neurobiology, 21(5), 1995, pp. 378-385
We have recently reported that sustained contraction of the canine bas
ilar artery induced by the intrathecal injection of talc (crystallized
hydrous magnesium silicate) mimicked delayed vasospasm following suba
rachnoid haemorrhage. The present study aims to examine the pathomecha
nism underlying talc-induced vasocontraction, from the viewpoint of fr
ee radical theory, which has been established as a cause of delayed va
sospasm. We estimated the effects of a prolonged intrathecal infusion
of human recombinant Cu/Zn superoxide dismutase (hr SOD) on the contra
ction of the basilar artery caused by the intrathecal injection of tal
c in beagle dogs, which were assigned to the three groups: G1, sham op
eration with saline treatment; G2, talc injection with saline treatmen
t; and G3, talc injection with 2 ml of hr SOD (7 x 10(4) U/ml) treatme
nt. Talc administration resulted in the reduction in the angiographic
calibre of the basilar artery by 63 and 61% on days 3 and 7 (G2), The
treatment with hr SOD (G3) led to a significant: attenuation of talc-i
nduced contraction of the basilar artery on days 3 (P<0.05 vs. G2) and
7 (P<0.05 vs. G2). In the basilar artery wall of days 3 and 7 in G2,
pathological changes such as myonecrosis, cytoplasmic vacuolation and
detached intercellular junctions were observed. However, these patholo
gical changes almost disappeared in G3. The present findings suggest t
hat superoxide anions may initiate and/or mediate talc-induced vasocon
traction and subsequent structural damage of the basilar artery.