Stroke, Vol 17, 207-213, Copyright © 1986 by American Heart Association
RP White
Blood proteins could play a critical role in the pathogenesis of cerebral
vasospasm in subarachnoid hemorrhage (SAH) as agonists and as antagonists
of vasoconstriction. The present study was designed primarily to quantify
the inhibition produced by antithrombin III of the phasic responses
elicited by cumulative doses of KCl, serotonin (5- HT), uridine
triphosphate (UTP), and thrombin in isolated canine basilar arteries, and
to ascertain whether other proteins might act similarly. Antithrombin III
(1 unit/ml and 3 units/ml) given 2 min beforehand inhibited all agonists.
The inhibition was not dependent on a functional endothelium nor due to
stimulation of the electrogenic sodium pump. Alpha2-macroglobulin (0.1
mg/ml and 0.4 mg/ml) inhibited the contractile responses to high K+, 5-HT
and thrombin. Kallikrein (1 and 4 units/ml) did not inhibit UTP but
inhibited high K+ and 5-HT through an effect on the endothelium. Kallikrein
(1 unit/ml) irreversibly blocked the responses to thrombin. Globulins (3
mg/ml) and fibrinogen (0.3 mg/ml) were not inhibitory. The results
demonstrate that anticoagulant proteins are very effective nonspecific
inhibitors of the vasoconstriction, whereas the serine protease kallikrein
selectively blocks thrombin. The remarkable potency of antithrombin III
suggests that it may protect cerebral arteries from exhibiting vasospasm in
SAH.
ARTICLES
Vasodilator proteins: role in delayed cerebral vasospasm
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