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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To elucidate the pathophysiology of intracardiac thrombus formation, serial two-dimensional echocardiographic examinations were performed on 30 consecutive patients with acute cardiogenic cerebral embolism in parallel with measurement of hematocrit and plasma levels of antithrombin III. The data from groups of patients with and without newly formed or enlarged thrombi were compared. Intracardiac thrombi were detected in eight of the 30 patients (27%), four at admission and four after admission. Enlargement of the thrombus was observed in four, and systemic embolization recurred in three of the eight. Antithrombin III levels already were low at admission in patients who later developed thrombi or had enlarged thrombi on serial examinations. When the development or enlargement of an intracardiac thrombus was detected by echocardiography, the diameter of the inferior vena cava was found to be reduced. At the same time, a decrease in antithrombin III and an increase in hematocrit were demonstrated. Intracardiac thrombi are frequently detected by repeated echocardiographic examination in patients with cerebral embolism. Dehydration seems to accelerate thrombus formation that is reflected by a decrease in antithrombin III. A low antithrombin III level at admission and/or a decrease in antithrombin III after admission may indicate the possible recurrence of embolism.
Stroke 1990 Jul
PMID:Predisposing factors of recurrent embolization in cardiogenic cerebral embolism. 223 65

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.
Stroke
PMID:Vasodilator proteins: role in delayed cerebral vasospasm. 242 60

98 post-menopausal women were randomly allocated to either Org OD 14 [(7 alpha, 17 alpha)-17-hydroxy-7-methyl-19-norpregn-5(10)-en-20-yn-3-one] 2.5 mg/day or placebo. Treatment was continued for up to 6 yr. Any thromboembolic episode that occurred was recorded. Prothrombin time (PT), partial thromboplastin time (PTT), factor VII level and factor X level were measured prior to treatment and at yearly intervals. Antithrombin III level was measured in the last two yr of the study. There was one cerebrovascular accident after 3 months of placebo therapy but no other thromboembolic episodes. No significant difference was found between the effects of Org OD 14 and placebo with regard to any clotting factors at any time interval, although factor VII and factor X levels were consistently lower in the OD 14 group than in the placebo group. Antithrombin III levels measured after 5 and 6 yr were significantly higher (P less than 0.01) in the OD 14 group, suggesting a reduced risk of thrombosis in the treatment group.
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PMID:Effects of long-term Org OD 14 administration on blood coagulation in climacteric women. 329 4

A deficiency of plasma antithrombin III has been identified as a potential risk factor for thrombosis. In a pilot study of 56 patients aged less than 40 years who presented with ischaemic stroke of unknown etiology, we detected only one case of plasma antithrombin III deficiency. Antithrombin III activity was estimated by a chromogenic assay. Hence, antithrombin III deficiency, though rare, should be considered while evaluating young patients with stroke of unknown etiology.
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PMID:Plasma antithrombin III deficiency in ischaemic stroke in the young. 1040 46