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)

Whole-blood fibrinolytic activity was measured in 68 pregnant and 29 nonpregnant women with a sensitive, solid-state assay in which 125I-labeled fibrin was bound to polystyrene tubes. Antepartum fibrinolytic activity in 36 normotensive gravid women [234.5 +/- 29.2 (mean +/- standard error of the mean) ng fibrin lysed/30 min] was significantly (p less than 0.001) greater than that found in 28 nonpregnant normotensive women not taking oral contraceptives (63.61 +/- 7.66 ng fibrin lysed/30 min) and not different from the activity observed during the active phase of labor (198.50 +/- 16.5 ng fibrin lysed/30 min.) Normotensive pregnant patients had a significant (p less than 0.001) increase in whole-blood fibrinolytic activity (341.04 +/- 25.7 ng fibrin lysed/30 min) within the first 24 hours after delivery which persisted in measurements taken the second postpartum day. Fibrinolytic activity values before labor, in the active phase of labor, and in the first and second postpartum days in 17 patients with mild to moderate pregnancy-induced or pregd or pregnancy-aggravated hypertension were not different from those found in the normotensive group. However, patients with severe pregnancy-induced or pregnancy-aggravated hypertension had significantly (p less than 0.01) lower levels of fibrinolytic activity than normotensive patients before labor, during the active phase of labor, and on the first and second postpartum days. The placental 800 X g and 110,000 X g fractions of patients with severe hypertension had a significantly (p less than 0.001) greater capacity to inhibit "in vitro" urokinase-induced fibrinolysis than similar fractions obtained from placentas of normotensive women, and there was a significant inverse correlation (r = 0.61; p less than 0.01) between whole-blood fibrinolytic activity and urokinase inhibition by placental fractions. Our findings indicate that contrary to widely held views, fibrinolysis is extremely active in term pregnancies and during labor and that a derangement of this activity is present in cases of severe pregnancy-induced or pregnancy-aggravated hypertension.
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PMID:Whole-blood fibrinolytic activity in normal and hypertensive pregnancies and its relation to the placental concentration of urokinase inhibitor. 42 17

Saline extracts were made from portions of 17 normal placentae and from 8 placentae from pregnancies complicated by fetal growth retardation, but not hypertension. The ability of these extracts to inhibit urokinase-induced fibrinolysis was measured using a fibrin plate technique. Placental extracts from pregnancies complicated by fetal growth retardation exhibited greater inhibition of urokinase-induced fibrinolysis. There was no evidence of disseminated intravascular coagulation in these patients, but certain coagulation factors in the peripheral blood were raised.
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PMID:Coagulation and fibrinolysis in pregnancies complicated by fetal growth retardation. 126 44

Urinary kallikrein and kallikrein activity significantly decreased in cases of preeclampsia (u-kall./CRE.index 42.39 +/- 9.66 ng/mg, u-kall. act./CRE.index 0.26 +/- 0.06 ng/min/mg), and urinary kininase II and kininase activity significantly increased (u-kininase/CRE.index 10.91 +/- 1.26 x 10(-3) IU/min/mg, u-kininase act./CRE.index 506.37 +/- 178.45 pg/min/mg) when compared with those of normal gravidas from 28 weeks to 42 weeks of gestation (u-kall./CRE.index 189.31 +/- 14.17 ng/mg, u-kall. act./CRE index 1.08 +/- 0.10 ng/min/mg, u-kininase/CRE.index 6.24 +/- 0.31 x 10(-3) IU/min/mg, u-kininase act./CRE.index 15.64 +/- 0.10 pg/min/mg). Urinary FPA, B beta 5-42, alpha 2-PI, and alpha 2PI-plasmin-complex (PIC) significantly increased in preeclampsia (u-FPA/CRE.index 23.59 +/- 8.47 ng/mg, u-B beta/CRE.index 105.26 +/- 29.30 ng/mg, u-alpha 2PI/CRE.index 121.53 +/- 43.57 ng/mg, u-PIC/CRE index 278.39 +/- 60.50 ng/mg) when compared with those of normal control group (u-FPA/CRE.index 0.92 +/- 0.04 ng/mg, u-B beta/CRE.index 12.15 +/- 0.44 ng/mg, u-alpha 2PI/CRE.index 4.18 +/- 0.33 ng/mg, u-PIC/CRE.index 5.98 +/- 1.15 ng/mg). Urinary urokinase markedly increased and urinary D-dimer was detected in severe cases of preeclampsia (u-UK/CRE.index 58.20 +/- 43.69 ng/mg, u-D-dimer 54.76 +/- 9.89 ng/ml) when compared with those of normal control group. These findings suggest that deficiency in urinary kinin excretion may induce hypertension in addition to the changes of urinary coagulation-fibrinolysis system that represents the occurrence of either the endothelial cell injury in the glomerulus or the renal tulbular damage in mild cases of preeclampsia, eventually resulting in the intra-renal vascular coagulation.
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PMID:Urinary coagulation-fibrinolysis, kallirein-kinin systems and kininase in cases of preclampsia. 133 34

An 80-year-old woman with acute myocardial infarct received intracoronary thrombolysis by a large dose of urokinase four hours after the onset of chest pain. Despite the patient having no chest pain after intracoronary thrombolysis and her general condition being stable, she died suddenly on the 4th hospital day. Autopsy revealed hemopericardium due to cardiac rupture, which occurred at the center of the transmural hemorrhagic infarction of the anteroseptal wall. The massive hemorrhagic infarction was promoted by reperfusion from thrombolytic therapy. She had also classic risk factors for cardiac rupture, such as hypertension, senility, female gender, and first acute myocardial infarct. Therefore, the present case demonstrated that hemorrhagic infarction increased the incidence of cardiac rupture.
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PMID:Cardiac rupture complicating hemorrhagic infarction after intracoronary thrombolysis. 141 60

Emergency coronary angiography in a 28-year-old male suffering an acute anteroseptal myocardial infarction revealed complete obstruction of the left anterior descending artery in association with multiple aneurysms of the 3 major coronary arteries. Successful intracoronary thrombolytic treatment with urokinase infusion directly into the infarct-related artery was performed 2 h after the onset. Follow-up left ventriculogram showed preservation of left ventricular wall motion. Fifty days after the infarction, he underwent aorto-coronary bypass surgery. Histological examination of the biopsy specimen obtained from the aneurysm of the distal portion of the right coronary artery revealed that the 3-layer architecture of the arterial wall had been completely lost. The wall was replaced by fibrotic tissue, with slight mononuclear cell infiltration around the small vessels, but no acute inflammatory reaction or atheromatous change was seen. In spite of the presence of the coronary risk factors of hypertension and hyperlipidemia, angiography revealed no evidence of atherosclerosis of systemic arteries. It is suggested that the coronary aneurysms in this case are possible sequelae of Kawasaki disease in childhood.
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PMID:Acute myocardial infarction in a young adult as possible sequela of Kawasaki disease--a case report of successful intracoronary thrombolytic therapy and histological study of an aneurysm. 149 60

We report a series of 10 patients who had a rapid expansion of a hypertensive intracerebral hemorrhage (HICH). It occurred in approximately 3% of 320 patients who sought treatment for HICH during the past 2 years. The site of hemorrhage was the putamen in 6 patients and the thalamus in 4 patients. Neurological deterioration occurred in a mean time of 40 hours after the onset of symptoms (range, 5.5-109 h). Fifty percent of all patients deteriorated within 24 hours. Persistent hypertension was recorded in all patients. Repeat computed tomography showed an increase of hematoma volume that was twice as large in thalamic hemorrhage and about three times as large in putaminal hemorrhage. Six patients died, whereas 3 survived with severe disability and 1 survived with moderate disability. This study indicates that continued or subsequent bleeding can occur in HICH. If those lesions are not detected early and microsurgically evacuated, they are almost always fatal. Early stereotactic evacuation with urokinase irrigation is considered more dangerous than open craniotomy by microsurgical techniques. We stress the need for attention to this problem during the acute phase of HICH.
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PMID:Rapid expansion of hypertensive intracerebral hemorrhage. 164 Nov 8

In the natural history of this disorder, resumption of normal activity after a period of recuperation (following an episode of thrombosis) frequently leads to symptoms of upper extremity venous hypertension exacerbated by using the arms in the overhead position. This position can be demonstrated venographically to further occlude collateral vessels in thoracic outlet. A number of patients develop more extensive symptoms of neurogenic thoracic outlet syndrome. Anticoagulation may protect the collateral vessels and interrupt the period of active clot propagation resulting in a better functional result than would be expected from the natural history of the thrombotic event. In our experience, local Urokinase was the most effective means for reestablishing venous patency. With clot dissolution the underlying compression of the vein at the thoracic outlet can be demonstrated. Balloon angioplasty should not be undertaken in the acute setting nor prior to relieving the tendinous compression. The acute phlebitic process should resolve under the protection of Coumadin for three months. At that time it can be determined more effectively which patients require additional therapy. Removal of the first rib will decompress the axillosubclavian vein and the thoracic outlet collaterals permitting the vein to regain its normal configuration particularly in younger patients with more acute onset of compression. In those patients with more chronic compression the vein becomes stenotic. Improvement of the luminal configuration has been accomplished with transvenous balloon angioplasty without the necessity for venous reconstructive procedures in this series. Patients with Paget-Schroetter syndrome have a symptom complex which often reflects more extensive neurovascular compression at the thoracic outlet than that which might result from venous hypertension alone. Although thrombolytic therapy can restore patency of the axillosubclavian vein, first rib resection is necessary to relieve the external compression. This procedure was very effective in patients who had restoration of subclavian vein patency, and to a lesser degree in those with residual occlusion.
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PMID:Effort thrombosis of the axillosubclavian vein: a disabling vascular disorder. 187 22

A 24-year-old white woman with a past history of recurrent venous thromboses of the lower extremities was admitted for hypertension and renal failure. She had a chronic cutaneous ulcer on the anterior side of the left leg and oral ulcers of the palatum. Laboratory tests demonstrated rapidly progressive renal failure and the presence of an anticardiolipin antibody (ELISA). Thrombosis of the inferior vena cava was shown by phlebocavography. Renal biopsy revealed typical thrombotic microangiopathy. Tissue-type plasminogen activator (tPA) was visualized by immunofluorescence in endothelial cells of renal arterioles and glomeruli. Normal plasma levels of tPA, urokinase and plasminogen activator inhibitor 1 were found by ELISA, and tPA antigen levels rose after desmopressin acetate infusion. Thus, in this case, the diffuse thrombotic process was not related to defective circulating or renal fibrinolytic systems and could be promoted by the procoagulant effect of antiphospholipid antibodies.
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PMID:Systemic and renal fibrinolytic activity in a patient with anticardiolipin syndrome and renal thrombotic microangiopathy. 211 23

Acute fatal pulmonary embolism is one cause of sudden death which should be guarded against. It is the most often missed diagnosis in sudden death cases within the hospital. Clinical pictures of 10 patients with acute fatal pulmonary embolism proved by autopsy were examined to elucidate the problems of diagnosis, and to look for an effective treatment, and a method of prevention. Common risk factors were old age and immobility due to stroke or postoperative state. Common past histories were hypertension, diabetes mellitus, obesity, atrial fibrillation and hyperlipidemia. Electrocardiogram and echocardiogram showed that in these patients there was definite evidence of acute right ventricular overload. High doses of intravenous urokinase should be given whenever acute cardiovascular collapse develops in such high risk patients. Emergent pulmonary angiogram and pulmonary embolectomy could be life-saving in patients with acute massive pulmonary embolism. Prevention is, however, the best treatment. In addition to anticoagulation medication, frequent change of body position and early mobilization are important precautions to prevent fatal pulmonary embolism developing in such patients.
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PMID:[Acute fatal pulmonary embolism: its prevention, diagnosis and treatment]. 236 72

Rapid inhibition of urokinase in plasma obtained from women in the third trimester of pregnancy was assessed by the addition of 75 IU urokinase per ml plasma, and measurement of residual urokinase activity with PyroGlu-Gly-Arg-pNA after 5 minutes incubation at 37 degrees C. The urokinase inhibitory capacity was markedly increased for the pregnant women compared to non-pregnant controls. Alpha 1-antitrypsin, alpha 2-macroglobulin and alpha 2-antiplasmin did not account for the activity. Inhibition was higher for women with multiple gestations or macrosomia (n = 11) compared to normal pregnant women (n = 35) suggesting that the placenta contributes significantly to the measured activity. Inhibition was lower for women with hypertension (n = 33) compared to the normal pregnant women. Although the etiology for this difference is unclear, the decreased inhibitory activity may contribute to the increased risk for placental abruption that is observed for this group of women.
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PMID:The rapid inhibition of urokinase by plasma from pregnant women at risk for abruptio placenta. 243 78


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