Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The records of 5 neonates with systemic arterial thrombosis (aortic in one case, peripheral in four cases) were reviewed. Fibrinolysis was performed with urokinase administered by infusion (1,000 to 4,000 U/kg/h). This treatment was combined with heparin therapy in 4 cases. Thrombosis was due to various causes: umbilical arterial catheter (1 case), disorders of supraventricular rhythm in utero (1 case), aneurysm of the ductus arteriosus with dysplastic aortic arch vessels (2 cases); one of these patients also had myocardiopathy. No cause could be found in a premature child weighing 1,300 g. The presenting symptoms of systemic arterial thrombosis are ischaemia of the extremities and suppression of peripheral pulses; heart failure with arterial hypertension is frequent. In our series the diagnosis was confirmed by doppler-ultrasonography in one case and by angiography in three cases (angiography in the left ventricule with foramen ovale, or umbilical aortography). Treatment with urokinase lasted 1.5 to 7 days. In 2 children the initial dosage had to be increased as there was no clinical improvement. Four children were completely cured; the fifth child, who had left renal thrombosis, shows slight functional impairment of the left kidney. There were no haemorrhagic complications. The fibrinolytic treatment with urokinase of systemic arterial thrombosis in the newborn is effective and has few drawbacks.
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PMID:[Treatment with urokinase of systemic arterial thrombosis in the newborn infant]. 250 Jan 1

Pulmonary embolism can produce severe cardiopulmonary dysfunction characterized by pulmonary artery hypertension, right ventricular failure, and hypoxemia. The search for the source of a pulmonary embolus, by exploration of the veins of the lower limbs and the inferior vena cava should be systematically carried out in all cases of pulmonary embolus which are not immediately life-threatening to the patient. The treatment of deep vein thrombosis associated with pulmonary embolism with thrombolytic agents has been proposed and utilized for approximately 20 years. Although superior results have been claimed with thrombolytic agents, the use of this type of treatment remains limited to massive or sub-massive pulmonary embolism. Fibrinolytic agents with high specificity for fibrin in the thrombi and little systemic activation of the fibrinolytic system have been developed and tested in preliminary clinical trials of patients with acute pulmonary embolism. The largest published experience available has been with recombinant tissue plasminogen activator (rtPA). The acylated streptokinase-plasminogen complex (APSAC) and pro-urokinase also gave promising results. All these agents were accompanied by unexpectedly high incidence of systemic activation of the fibrinolytic system and by hemorrhagic complications with frequencies similar to those that follows the use of first generation products (urokinase and streptokinase). Hence, their superior clinical efficacy must be clearly proven before they are substituted for a more widely available and less expensive drug, such as streptokinase.
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PMID:Pathogenesis and management of acute pulmonary embolism. 251 49

A case of microangiopathic hemolytic anemia (MHA) associated with the immunosuppressive agent, cyclosporine, is reported herein. The patient manifested anemia with red blood cell fragmentation, hypertension, thrombocytopenia, elevation of serum LDH levels and glomerular capillary thromboses within a few days of his transplantation. Extensive treatments with urokinase and heparin proved ineffective and graftectomy was performed 7 days after his transplantation. Immunofluorescent staining failed to show immunoglobulin (IgG or IgM) or complement (C3) deposition within the glomeruli, which discriminated MHA from acute humoral-vascular rejection.
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PMID:Cyclosporine-associated microangiopathic hemolytic anemia in a renal transplant recipient. 265 53

232 consecutive patients with acute myocardial infarction were treated either with 2 x 10(6) IU urokinase as an intravenous bolus injection, or 250,000 IU streptokinase intracoronary, or 60 mg recombinant tissue-type plasminogen activator (rt-PA) over 90 min. All patients enrolled had chest pain for more than 30 min and less than 3 h before admission and a typical electrocardiogram. Contra-indications to thrombolytic treatment were absent. All bleeding complications occurring within 24 h after admission were assumed to be due to thrombolytic therapy. Bleeding complications occurred in 14 patients (6.5%). Only seven patients received a blood transfusion (3%). No correlation was evident between previous hypertension, diabetes mellitus, smoking, sex, age, fibrinogen level before and 24 h after thrombolytic therapy and bleeding complications. The risk of bleeding was not significantly different between the different thrombolytic regimens despite marked differences in the fall of the fibrinogen level. The decrease of fibrinogen following thrombolytic therapy did not influence the patency rate of the infarct vessel. Thrombolytic therapy in acute myocardial infarction is a safe treatment even among patients advanced in years and with medically controlled hypertension and diabetes mellitus, irrespective of the kind of thrombolytic treatment.
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PMID:Bleeding after thrombolysis in acute myocardial infarction. 270 62

The accepted correct procedure for treating occlusive arterial diseases includes surgical disobstruction, CL as well as PTA. Combined non-surgical strategies are effective in about 60% of these patients. However, a high risk of rethrombosis despite from the prophylaxis with anticoagulants like heparin or antiplatelet drugs like ASA is proven, especially in patients with multi-segmental stenosis as well as in patients with extensive narrowing of the arteries. In these cases primary lesions (endangitis obliterans) or secondary lesions of the endothelium cause local depletion of plasminogen in the endothelium. Independent of the method used for reopening the vessel in these patients, a significant progression of the vessel disease and a high rethrombosis rate during longterm follow-up is observed. These results lead us to apply plasminogen locally to decrease the rate of rethrombosis. In patients suffering from stage III-IV (La Fontaine) including patients with multi-segmental stenosis as well as extended narrowing of the artery, PTA in combination with CL was performed. The catheter was placed as near as possible to the thrombus. In some cases the 'fibrinolyticum' could be injected directly into the thrombus. In these cases a bolus of 4,000 U/ml was locally infused, otherwise 1.0-1.5 million U urokinase per 24 hrs. were locally infused with heparin. In 28% (22 patients) no sufficient clinical response occurred using this combined therapy and plasminogen was applied locally. The following criteria supported our decision to include the patients in this study: 1. Insufficient response occurring after 12-24 hrs. of local infusion. 2. Following 6 bolus injections no reopening of the vessel occured within 60 minutes or the clinical response was insufficient due to rethrombosis. 3. Insufficient effects of lysis therapy after 2 hours and contraindication for a systemic fibrinolytic therapy (e.g. hypertension, age, etc.). 1,000 U plasminogen per ml were infused locally or 2,000 U up to 5,000 U plasminogen (in 5 to 10 ml 0.9% saline) were infused slowly (2-4 minutes infusion time) into the catheter in these patients 10 minutes after unsuccessful treatment with local urokinase therapy. Five minutes after administering plasminogen local intraarterial fibrinolytic therapy with urokinase was continued. No severe side effects due to this therapy were observed, although some patients suffered from acute pains in the peripheral segments of the arteries occurring immediately after infusion of plasminogen. In 16 of 22 patients a complete recanalization occurred and in 3 patients a satisfying clinical improvement was observed.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effectiveness of intraarterial plasminogen application in combination with percutaneous transluminal angioplasty (PTA) or catheter assisted lysis (CL) in patients with chronic peripheral occlusive disease of the lower limbs (POL). 296 85

In eight male patients with normal liver and kidney function fibrinolytic components were measured in arterial blood and in renal and hepatic vein blood, obtained during catheterization for analysis of hypertension. Blood samples were collected simultaneously from veins und corresponding arteries before and 5 minutes after the completion of intravenous injection of desmopressin (DDAVP), 0.4 micrograms/kg body weight over a 10 minute period. DDAVP induced a rise in t-PA antigen and activity, and in von Willebrand factor, accompanied by a decrease in free PA-inhibitor level. We failed to detect a significant rise in plasma urokinase activity. The concentrations of fibrinogen, plasminogen, alpha 2-antiplasmin, antithrombin III and coeruloplasmin did not change either. Renal production of t-PA under basal conditions was inferred from a negative arterio-venous (A-V) difference in t-PA-activity and in t-PA-antigen levels but this could not be confirmed by orthogonal regression analysis of the same data. A-V differences of other fibrinolytic factors were negligible. In the hepatic vessels a significant positive A-V difference of t-PA-activity and of t-PA-antigen levels was a uniform finding. After DDAVP, when plasma levels were elevated, the mean A-V difference was proportionally higher, consistent with a constant fractional elimination rate. Free PA-inhibitor was virtually absent from arterial blood after DDAVP, but appeared in hepatic vein blood, indicating either production of the inhibitor by the liver or dissociation of a circulating complex of t-PA and its inhibitor in the liver. The blood levels of the other investigated components did not show any change upon passage through the liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and hepatic handling of endogenous tissue-type plasminogen activator (t-PA) and its inhibitor in man. 314 78

In the past 20 years treatment appears to have had a major impact on all forms of cerebral vascular disease. Morbidity and mortality from strokes have declined nearly 50% in developed countries. Modern imaging techniques, methodology, and biostatistics have identified risk factors and refined clinical trials such that we question all previous studies of stroke management. Control of moderate and severe hypertension has significantly lowered stroke rates. In borderline and mild hypertension the decision to treat is influenced by other stroke risk factors including diabetes mellitus, cigarette smoking, ischaemic heart disease, plasma lipid levels, gout, haematocrit, and body weight. Current data indicate that anticoagulants are of no value, or hazardous, in atherothrombotic strokes; of unknown value in transient ischaemic attacks; of dubious value in evolving strokes; and beneficial in cardiac embolism. The cardiac causes, including mural thrombus, unstable arrhythmias, and mitral valve prolapse should be actively sought. Aspirin, as the prototype anti-platelet agent, holds promise in transient ischemic attacks and minor strokes at both small and moderate dosages. Ticlopine is now being critically evaluated in America. Use of cerebral vasodilators should be abandoned. Enthusiasm in the use of streptokinase and urokinase has been dampened by the conversion of ischemic infarcts into haemorrhagic infarcts. In subarachnoid haemorrhage epsilon-aminocaprioc acid is useful although hazardous, in preventing rebleeding. Certain calcium ion channel blockers are promising in the reduction of vasopasm. Since the November 1985 article in the new England Journal of Medicine on the failure of external-to-internal carotid arterial bypass to reduce the risk of ischemic stroke, the swing is back to conservative management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Advances in the medical management of cerebral vascular disease. 331 47

Fibrinogenolysis induced by thrombolytics exposes the risk of haemorrhagic complications. The efficacy is proved for pulmonary emboli of recent origin. The aim of this study is to research into the effect of local administration of low dose urokinase in six patients aged 40 (+/- 16 years) and presenting with old emboli (10 +/- 4 days). The initial clinic picture was serious with shock (2 cases), hypoxaemia (6 cases), pulmonary arterial hypertension (mean 40 +/- 8 mmHg) and a Miller index of 58 (+/- 8%). Mechanical ventilation was necessary four times. Urokinase was administered in situ using a Swan Ganz catheter, with 1,000 units per Kg per hour for six hours followed in sequence with 30 microkatals per hour of plasminogen for two hours. This eight hourly rotating sequence was followed for at least 72 hours. Six patients were cured with an end of treatment (5 +/- 2 days) improvement in their hypoxaemia of 22%, a fall of 47% of the pulmonary arterial pressure and a rise of 71% in the Miller index. The fibrinogenesis fell by 11% and the thrombolytics could not blamed for any side-effect. The sequence urokinase-plasminogen in low dose administered locally may represent an alternative treatment for severe and long standing pulmonary emboli in patients with a risk of haemorrhage.
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PMID:[Value of thrombolysis in situ without general fibrinogenolysis in pulmonary embolisms of more than 5 days duration]. 344 74

Monoclonal antibodies to purified human urinary kallikrein have been developed. Selection of antibody producing clones was based on 125I-kallikrein binding activity of hybridoma media in both radioimmunoassay and enzyme-linked immunosorbent assay. Three clones (2 IgG1, 1 IgG2b) were subcloned, characterized, and compared with the polyclonal antiserum generated in rabbits immunized with the purified kallikrein. With radioimmunoassay, mouse ascitic fluids or rabbit antisera dilutions showing 50% binding to 125I-kallikrein were 1:1.2 X 10(6) (E7A9), 1:1.2 X 10(5) (H6A6), 1:8.0 X 10(4) (E12H1), and 1:1.4 X 10(6) (the rabbit antisera). With enzyme-linked immunosorbent assay, mouse ascitic fluids from clones E7A9 and H6A6 showed half-maximal absorbance at dilutions of 1:2.1 X 10(5) and 1:1.0 X 10(5) respectively, and the polyclonal antiserum showed half-maximal absorbance at a dilution of 1:2.0 X 10(4). These monoclonal antibodies showed no cross-reactivity with rat tissue kallikrein, rat urinary plasminogen activator, or dog pancreatic kallikrein, while the polyclonal antiserum showed some cross-reactivity. The binding of monoclonal or polyclonal antibodies to 125I-human urinary kallikrein was not affected by human plasma kallikrein, thrombin, or urokinase in a competitive radioimmunoassay. By using purified human urinary kallikrein immobilized to agarose, antibodies produced by clones E7A9 and H6A6 and in the rabbit antisera were purified to homogeneity. Each of these affinity-purified antibodies inhibited the esterase activity, and two of the three inhibited the kininogenase activity, of human urinary kallikrein. A sandwich immunosorbent assay was developed to measure this kallikrein using monoclonal antibody from the clone E7A9 in conjunction with the polyclonal antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Characterization of monoclonal and polyclonal antibodies to human tissue kallikrein. 385 80

A patient with systemic lupus erythematosus had severe hypertension, rapidly worsening renal failure, and multiple successive thrombotic cerebrovascular and retinal lesions develop. In a kidney biopsy specimen luminal thrombi were demonstrated in arteries and arterioles, without vasculitic or inflammatory changes. The patient's plasma was markedly deficient in both prostacyclin stimulating factor (PSF) and vascular plasminogen activator (VPA), and also contained a potent inhibitor of in vitro urokinase-induced fibrinolysis. Treatment with ancrod resulted in striking reversal of the progressive renal damage and clinical recovery from the thrombotic cerebrovascular and retinal lesions. This clinical improvement was associated with improved renal histologic appearance, correction of the PSF and VPA deficiencies, and disappearance of the urokinase inhibitor. Possible mechanisms of action of ancrod are discussed.
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PMID:Ancrod in systemic lupus erythematosus with thrombosis. Clinical and fibrinolysis effects. 622 28


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