Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Radiographically verified spontaneous disappearance of medium-sized arterial cerebral aneurysms is seldom reported, and only three times in connection with antifibrinolytic therapy (EACA). In our clinic repeat angiograms have shown non-filling of the aneurysms in three patients during treatment with tranexamic acid (AMCA) two, three, and four weeks respectively after primary bleeds. Initially, all three patients had severe radiological vasospasm associated with neurological deterioration. Follow-up angiograms have demonstrated partial reappearance of the aneurysm after one month in one patient and complete disappearance of the aneurysms in the other two patients after 9 and 22 months respectively. In two cases occlusion of cerebral arteries occurred. With regard to the higher risk of severe vasospasm and occlusion of cerebral arteries in our opinion it should not be a therapeutic goal to try to achieve a thrombosis of a ruptured aneurysm with antifibrinolytic drugs. The reason for spontaneous aneurysm thrombosis during treatment with AMCA may be a local inhibition of plasminogen activators in and around the aneurysm wall. It may also be related to the sympathomimetic property of the drug, with vasospasm and a subsequent flow-reduction inside the aneurysm or a possible interaction with other drugs and substances.
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PMID:Spontaneous thrombosis of ruptured intracranial aneurysms during treatment with tranexamic acid (AMCA). Report of three cases. 51 75

It has been established that patients with duodenal ulcer complicated by hemorrhage in the past are characterized by the low response of the fibrinolytic system (FS) to two different exposures--local venous occlusion and administration of the sympathomimetic alupent. The rate of plasminogen the lower limit of normal in almost 2/3 of patients with activator release (RPAR) from vascular depots was under hemorrhages and in 1/4 of those with uncomplicated duodenal ulcer. The low RPAR was coupled with hereditary aggravation and hyperplasia of the parietal glandulocytes of the stomach. In duodenal ulcer complicated by hemorrhages, the normal parameters of the fibrinolysis kinetics and RPAR were encountered 3 times less frequently than in uncomplicated duodenal ulcer, whereas activated blood fibrinolysis coupled with the low RPAR 5 times as frequently. The shifts can severe a discriminant prognostic criterion painting to a potential risk of hemorrhage and making it possible to carry out the different prophylaxis. The treatment with epsilon-aminocaprotic acid given in courses makes the FS including its vascular component return to normal.
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PMID:[Vascular component of the fibrinolytic system of blood (plasminogen activator of vascular wall) in patients with duodenal ulcer with a history of hemorrhagic complications]. 404 Jun 57