Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

Between 1984 and 1989, 35 patients with recent arterial or graft occlusions have been treated with intra-arterial infusion using sequential association of Urokinase (U.K.) and Lys-Plasminogen. Occlusion was thrombotic in 68.5% of the cases ans embolic in 31.5%, involving 28 native arteries and 7 bypass grafts. The mean duration was 16 days (2 to 90). Continuous infusion of U.K.: 84,000 U.I./H and bolus of Lys-Plasminogen 15 microKatals every 30 minutes were delivered through a catheter embedded into the clot. Intra-venous heparin was always associated. The mean duration of lytic drug infusion was 8 H. Complementary arterial reconstruction by vascular surgery of percutaneous transluminal angioplasty was performed in 23% of the patients. Patients with recent alimentary tract bleeding, hemorragic stroke in the last six months or severe high blood pressures were contra-indicated. Complete lysis was obtained in 23 cases (66%), partial lysis in 7 (20%) and no lysis in 5 (14%). The clinical result was excellent in 24 cases (68.5%), good in 3 (8.5%) and bad in 8 (23%) in which amputation was always necessary. 5 local hematoma (14%) treated by surgery or transfusion and one death (3%) due to neurological complication occurring 24 hours after the end of the procedure were observed. The literature survey has shown that the results of low doses of Streptokinase (S.K.) local infusions were not better, and that higher doses of S.K. or U.K. delivered during a shorter infusion time increased the efficacy of lysis and decreased the rate of hemorragic complications. We have proposed the local thrombolytic treatment to the limb threatening ischemic cases when the traditional medical or surgical techniques where thought to be associated to a high risk of failure or complication. The specific indications are the acute or sub-acute ischemic situation due to atheromatous artery thrombosis, distal or old embolism where the Fogarty catheter is inefficient, and graft thrombosis. Severe acute ischemia with neurologic involvement are not good indications. Local thrombolysis can be successful on arterial occlusion even after one month duration.
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PMID:[Intra-arterial thrombolytic therapy of lower limb ischemia]. 237 17

Thrombolytic recanalization of arterial bypass grafts has been pursued aggressively in the peripheral circulation but not in the coronary circulation. In an attempt to apply peripheral transcatheter thrombolytic techniques to the coronary circulation, nine patients with 10 occluded saphenous aortocoronary bypass grafts underwent recanalization procedures using a short-duration, high-dose urokinase infusion. Urokinase was infused at the occluded graft orifice at a rate of 600 units/min. The average infusion time was 1 hr, 26 min. The average urokinase dose was 435,000 units. Graft recanalization was achieved in eight (80%) of 10 grafts, although only six (60%) of 10 grafts were widely patent at the end of the procedure. All successfully recanalized grafts required balloon angioplasty of underlying stenoses. No complications, specifically myocardial infarction or cerebrovascular accident, were encountered. We have shown that occluded aortocoronary bypass grafts can be recanalized successfully by using a short-duration, high-dose urokinase infusion. It appears that, with attention given to angiographic techniques that minimize clot manipulation, recanalization can be accomplished safely in a majority of cases.
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PMID:Short-duration, high-dose urokinase infusion for recanalization of occluded saphenous aortocoronary bypass grafts. 278 70

Since the majority of ischaemic cerebral infarcts is caused by thromboemboli, we determined the benefit of fibrinolytic therapy in acute stroke. Thromboemboli were induced in the middle cerebral artery of 21 dogs. Urokinase was started at different time intervals after infarction (1, 3 and 5 hours) at a rate of 1000 IU/kg/min. Angiographically controlled thrombolysis was achieved in all 15 treated cases, whereas in the control group (n = 6) no case of recanalisation was observed. Systemic fibrinolysis occurred in all cases. Postmortem examinations of the brains showed no intracerebral haemorrhages. Our findings indicate that urokinase treatment may be of value in acute ischaemic stroke.
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PMID:[Experimental thrombolysis of thromboembolisms in the middle cerebral artery circulatory area]. 283 70

In 16 patients with recent myocardial infarction (3 to 12 week old) and with large left ventricular thrombi systemic thrombolysis with urokinase was performed. Left ventricular thrombi were diagnosed by two-dimensional echocardiography; in all patients the mural thrombus was located in the area of recent myocardial infarction. Each of three patients suffered an embolic episode before the initiation of thrombolytic therapy and the episode caused a stroke in one. Urokinase was infused intravenously at a rate of 60,000 U/hr for 2 to 8 days in combination with intravenous heparin (200 units/kg X 12 hr). Left ventricular thrombi were successfully lysed in 10 of 16 patients, as determined by two-dimensional echocardiography. In four of the six remaining patients only partial thrombolysis was achieved and in two thrombolytic treatment failed. There was no evidence of embolic events during thrombolysis in any of the 16 patients. The success of thrombolysis seemed to depend on the age of the thrombus: the thrombus was dissolved in eight of nine patients undergoing thrombolysis within 4 weeks of the acute myocardial infarction vs in two of seven patients receiving treatment later (p = .057). The presence of a left ventricular aneurysm or depressed left ventricular function also appeared to reduce the likelihood of successful thrombolysis. All patients were discharged on oral anticoagulants. At 6 months follow-up (n = 9) no recurrence of left ventricular thrombus was found. These results show that left ventricular thrombi can be safely lysed by intravenous urokinase. However, for better definition of the risk and benefit of this new therapy further investigation is necessary.
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PMID:Lysis of left ventricular thrombi with urokinase. 400 22

A successful case undergoing the ECA-PCA bypass operation with the use of an interposition saphenous venous graft for vertebrobasilar progressing stroke was reported and details of the operative techniques were described. A 40-year-old man was admitted because of confused mental state following sudden onset of headache, vomiting, vertigo, and ataxic gait. Neurological examinations revealed he was confused and restless, and left-sided Weber's syndrome, bulbar palsy and dysphasia were noticed. CT scan showed multiple small low density areas with no enhancement scattering in both occipital lobes and cerebellar hemispheres. Angiographical studies showed that the left vertebral artery was occluded at the vertebrobasilar junction and the right vertebral artery stenosed up to 90% or more at the branching site of the PICA. There was no visualization of the vertebrobasilar system through the right posterior communicating artery. The left posterior communicating artery was not examined. The patient was treated with Urokinase amounting to 740,000 units for ten days. Thirteen days later, however, he became progressively drowsy and he became unable to speak and swallow. Quadriparesis also appeared. Progressive deterioration of these brain stem ischemic symptoms was assumed to originate from critically lowered perfusion of the vertebrobasilar circulation. Therefore, the ECA-PCA anastomosis by means of a venous graft was carried out on the right side in expectation of the rapid restoration of the blood flow in the affected brain stem. A venous graft was chosen because it would carry larger amount of blood immediately after completing the bypass surgery than small calibered arterial graft such as a superficial temporal artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ECA-PCA anastomosis with the use of an interposition saphenous vein graft for vertebrobasilar progressing stroke]. 404 16

Seven prospective, epidemiological studies indicate plasma fibrinogen levels (over 300-350 mg/dl) as an important, independent cardiovascular risk factor for subsequent myocardial infarction and stroke. Furthermore, several clinical studies revealed an association between fibrinogen and both the angiographic and clinical degree of coronary heart disease. In addition, a significant relation of fibrinogen with the number of occluded coronary vessels was found. The following pathophysiologic mechanism are of particular importance: Fibrinogen is a main determinant of plasma viscosity and red cell aggregation. Both phenomena deteriorate blood fluidity especially in the microcirculation. Fibrinogen plays a central role in platelet aggregation and performs an essential substrate in the coagulation cascade. Thus, high fibrinogen levels may favor a hypercoagulable state resulting in final thrombotic events of cardiovascular disease. Fibrinogen is also involved in atherogenesis by stimulating proliferation and migration of smooth muscle cells. Several determinants of fibrinogen levels are known. Smoking is the strongest one in healthy persons. This clinically important effect is dose related. Consequently, cessation of smoking is a major step to lower fibrinogen and subsequently the individual cardiovascular risk. Reduction of overweight and maintenance of regular physical activity are further nonpharmacologic means. Fibrates decrease fibrinogen about 10-30% on an average. Finally, intermittent low-dose Urokinase for end-stages of coronary artery disease and LDL-apheresis (HELP) represent additional approaches to reduce fibrinogen.
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PMID:[Clinical significance of the cardiovascular risk factor fibrinogen in secondary prevention]. 776 17

Thrombolytic therapy has been proposed in the treatment of cerebrovascular occlusive disease. Early clinical experiences with Urokinase and Streptokinase raised concern about the risk of hemorrhagic complications. More recently, tissue plasminogen activator (tPA) has been evaluated experimentally with promising results. Its clinical utilization has been recently initiated. A review of experimental and clinical data on thrombolysis in cerebral ischemia is presented. TPA treatment produced recanalization and clinical improvement in several patients. The rate of intracranial hemorrhagic complications is similar to the incidence of spontaneous hemorrhagic conversion of ischemic infarction. Nevertheless, large placebo-controlled clinical trials are necessary to further define the efficacy and the optimal modality of administration of tPA in thromboembolic stroke.
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PMID:Thrombolysis in cerebral ischemia. A review of clinical and experimental data. 830 72

The 4 widely available thrombolytic agents, alteplase (recombinant tissue plasminogen activator, rt-PA), anisoylated plasminogen streptokinase activator complex (APSAC; anistreplase), streptokinase and urokinase have revolutionised the treatment of acute myocardial infarction and are also effective in treating pulmonary embolism and peripheral arterial thrombosis. Therapeutic efficacy of the agents appears to be similar. Choice of a thrombolytic agent depends more on patient characteristics, availability and familiarity with the drug, cost and differences in tolerability. While overall thrombolytic therapy is relatively safe, these 4 agents differ in their tolerability profiles. Streptokinase has the lowest cerebral haemorrhage rate, anistreplase an intermediate and alteplase the highest rate. The incidence of total stroke is also higher with alteplase and anistreplase than with streptokinase, translating to an actual difference in patient risk of 4 extra strokes per 1000 patients treated. Risk of major bleeding is dependent on predisposing factors and seems to be similar with each agent. The incidence of hypotension with alteplase (4.3% in ISIS-3) is less than with streptokinase or anistreplase (6.8 and 7.2%, respectively in ISIS-3). The incidence of major anaphylactic reactions with streptokinase and anistreplase is low (< 1%). Urokinase and alteplase may be preferred for readministration of thrombolytic therapy and anistreplase is the agent of choice where rapid completion of therapy is desirable. The various agents may have different tolerability profiles with different adjunctive therapies and further data are therefore required.
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PMID:Comparative tolerability profiles of thrombolytic agents. A review. 847 Nov 85

Cerebral infarction initiates a cascade of molecular events, leading to proteolytic cell death. Matrix-degrading metalloproteinases (MMPs) are neutral proteases involved in extracellular matrix damage. Type IV collagenase is an MMP that increases cerebral capillary permeability after intracerebral injection and may be important along with plasminogen activators (PA) in secondary brain edema in stroke. Therefore, we measured MMPs and PAs in spontaneously hypertensive (SHR) or Wistar-Kyoto (WKY) rats with permanent middle cerebral artery occlusion (MCAO). Brain tissue was assayed for MMPs and PAs at 1, 3, 12, and 24 h and 5 days after occlusion, using substrate gel polyacrylamide electrophoresis (zymography). SHR showed an increase in 92-kDa type IV collagenase (gelatinase B) in the infarcted hemisphere compared with the opposite side at 12 and 24 h (p < 0.05). Gelatinase A remained the same in both infarcted and normal tissue until 5 days after injury, when it increased significantly (p < 0.05). Urokinase-type PA was increased significantly at 12 and 24 h and 5 days, while tissue-type PA was decreased significantly at 1, 12, and 24 h in the ischemic compared with the nonischemic hemisphere. Gelatinase B was markedly increased in SHR at 12 and 24 h compared with WKY (p < 0.05). Secondary vasogenic edema is maximal 1-2 days after a stroke, which is the time that gelatinase B was elevated. The time of appearance of gelatinase B suggests a role in secondary tissue damage and vasogenic edema, while gelatinase A may be involved in tissue repair.
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PMID:Proteolytic cascade enzymes increase in focal cerebral ischemia in rat. 862 40

The clinical effects were compared between a thrombolytic agent (urokinase) and a thromboxane synthetase inhibitor (sodium ozagrel) in patients with acute lacunar infarction. All patients had some degree of neurological deficits, which corresponded to the lesions on computerized tomography or magnetic resonance imaging. Urokinase of 420,000 units was given over two days in 11 patients, 160 mg/day of sodium ozagrel was administered for two weeks in 23 patients. The study was followed up to one month after the onset. Urokinase treatment improved motor paresis in 45.5-62.5% of the patients, sodium ozagrel in 68.4-86.7%. Using the combined score of motor paresis and conscious disorder, urokinase group revealed 44.4-45.5% improvement, but sodium ozagrel group 81.0-89.5% (p < 0.05). The rates of suppressive effect in progressing stroke and complete recovery were higher in sodium ozagrel group. Sodium ozagrel was clinically more efficient than urokinase in patients with lacunar infarction.
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PMID:[Clinical effects of urokinase and sodium ozagrel in patients with acute symptomatic lacunar infarction]. 888 28


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