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)

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

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

Complete recanalization was achieved by intra-aortic infusion of urokinase in a case of complete occlusion of the abdominal aorta. The patient was a fifty-nine-year-old man with atrial fibrillation, hypertension, and diabetes mellitus who was admitted because of intermittent claudication and pain in both lower extremities at rest. Angiography demonstrated complete obstruction of the abdominal aorta, but the bilateral iliac arteries were visualized via collaterals. Urokinase was administered intra-aortically in a total dose of 1,200,000 U during the first day and a total dose of 960,000 U during the second day. The aorta and the iliac arteries recanalized after this treatment, and complete recanalization associated with disappearance of subjective symptoms was observed after one month of treatment with warfarin. The present case suggests the usefulness of intra-arterial infusion of urokinase for the treatment of complete occlusion of the abdominal aorta.
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PMID:Complete recanalization of total occlusion in abdominal aorta by intra-aortic infusion of a thrombolytic agent--a case report. 832 87

Fifty-six occluded iliac arteries (mean length 6.1 cm; range 1-17 cm) in 50 patients were treated by percutaneous transluminal angioplasty (PTA) or laser-assisted PTA (bilateral lesions in 6 patients). Twenty-seven patients (54%) were at high risk for surgery. Patients were followed for a maximum period of 72 months (mean 23.12 months; median 20 months). The initial success rate was 78.57% for arteries and 82% for patients. Laser-assisted PTA was attempted in 11 occluded arteries (19.64%) and was successful in 4 arteries (7.14%). Conventional PTA was successful in 71.4% of arteries including all 7 arteries for which laser-assisted PTA failed (76% of patients). PTA was unsuccessful in 12 arteries (21.43%). Urokinase was used before PTA in 1 artery. The effect of PTA was evident clinically by relief of rest pain (66.66%), healing of ulcer (57%), increased claudication distance or no claudication (79%) in limbs, and objectively, by improvement in ankle/arm index (AAI) (an increase of 0.16 to 0.91) and increased exercise tolerance. Continuous improvement in AAI was observed after PTA on follow-up in 9 limbs. One patient died during follow-up. On follow-up, 3 arteries were occluded, 6 showed evidence of stenosis, and 1 showed fusiform dilatation at the PTA site. The long-term results using the life-table method determined a 76% primary patency rate and 81% secondary patency rate for 72 months. The overall patency including failures was 63%. Age of the patients (p = 0.0169) and hypertension (p = 0.0015) significantly affected the long-term patency of the artery but not the initial success. The major complications were arterial rupture in a repeat procedure in 1 artery, axillary artery thrombosis in 1, and distal thromboembolic occlusion during PTA in 4. The long-term patency rates suggest that PTA of totally occluded iliac arteries is a safe and effective procedure and provides a long-term benefit.
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PMID:Total occlusion of iliac arteries: results of balloon angioplasty. 833 88

Surgical thrombectomy is not a rational approach to neonatal renal vein thrombosis since the occlusion mainly involves intrarenal branches rather than the main renal vein, which is even patent in some instances. Conservative management combines supportive therapy for renal failure and systemic hypertension, if needed, and either heparin or thrombolytic agents. Streptokinase has proven difficult to handle in neonates and should not be used. Urokinase has been used in 18 patients but results are difficult to interpret because these cases occurred over an 18-year period. Plasminogen tissue activator, the latest thrombolytic agent developed, has been used in few pediatric patients. An international task force is currently studying whether or not a randomized study is warranted to provide data for standardizing thrombolytic therapy in pediatric renal vein thrombosis.
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PMID:[Treatment of renal vein thromboses in the newborn]. 845 33

The purpose of this study was to evaluate the efficacy of direct intra-arterial Urokinase infusions prior to anticipated adjunctive reconstructive vascular procedures in 16 patients with 24 acutely or subacutely occluded lower extremity grafts (22 femoropopliteal, 2 femorotibial). Complete thrombolysis was achieved angiographically in 18 (75%) of 24 graft occlusions. Neither age, gender, current smoking, diabetes mellitus, hypertension, nor coronary arterial disease were significantly associated with complete thrombolysis. The only significant factor related to complete thrombolysis was the duration of the occlusion prior to lytic treatment (p < 0.05). Adjunctive reconstructive procedures were performed for eleven of 18 cases in which complete thrombolysis was achieved. These included nine percutaneous transluminal balloon angioplasties (at eight distal and one proximal anastomotic stenoses) and two bypass operations (femoropopliteal). The remaining seven cases had no adjunctive procedure. These 18 cases were examined for patency rates during nine months of follow-up. Six (54%) of 11 cases with adjunctive reconstructive vascular procedures remained patent, while one (14%) of seven cases with no adjunctive procedure remained patent (p = 0.1). Six (25%) of 24 cases resulted in incomplete thrombolysis. Vascular procedures following these cases included two bypass operations, three amputations and one sympathectomy. This study suggests that complete thrombolysis of acutely occluded grafts might have minimized subsequent reconstructive procedures. Identification of correctable lesions and adjunctive reconstructive procedures performed following complete thrombolysis may be the important factors related to long-term patency.
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PMID:Thrombolytic therapy before reconstructive vascular procedures for acute or subacute graft occlusions. 847 85

Life-threatening, complete middle cerebral artery infarction occurs in up to 10% of all stroke patients. The "malignant media occlusion" is an infarction occupying more than 50% of middle cerebral artery territory. The malignant, space-occupying supratentorial ischemic stroke is characterised by a mortality rate of up to 80%. Several reports indicate, that hemicraniectomy in this situation can be life-saving. Hemicraniectomy increases cerebral perfusion pressure and optimises retrograde perfusion via the leptomeningeal collateral vessels. A case of a patient is presented, having progressive neurological deterioration due to massive cerebral infarctions. The patient rehabilitation was successful. Decompressive surgery is life saving and can also give acceptable functional recovery. Hemorrhagic stroke is due to stroke in 15% of cases and in 10%, it is "spontaneous" intracerebral hematoma. The intracerebral and intraventricular hemorrhage represents one of the most devastating types of stroke associated with high morbidity and mortality. The 30-day mortality rate is 35% to 50% and most survivors are left with a neurological disability. The value of surgical therapy is debatable. The aspiration and urokinase therapy of the hematoma of intracerebral hemorrhage could improve final neurological outcome. Spontaneous, nontraumatic intraventricular hemorrhage frequently carries a grave prognosis. A large part of morbidity after intraventricular hemorrhage is related to intracranial hypertension from hydrocephalus. One patient presented had intracerebral hemorrhage and another had intraventricular hemorrhage treated with urokinase. Rapid and extensive reduction in the amount of intracerebral and intraventricular blood occurred. Urokinase lysis is safe and can be a potentially beneficial intervention in intracerebral and intraventricular hemorrhage. By performing decompressive craniectomy, the neurologists of stroke departments and intensive care units with the neurosurgeons will have to play major role in the management of stroke patients.
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PMID:[New methods of intensive therapy in stroke: hemicraniectomy in patients with complete middle cerebral artery infarction and treatment of intracerebral and intraventricular hemorrhage with urokinase]. 1212 81

Chronic renal allograft rejection is often associated with the presence of fibrin thrombi in the microcirculation. Our purpose was to evaluate the influence of chronic rejection on fibrinolytic regulators in plasma of renal allograft recipients. We evaluated the concentration and activities of tPA, uPA and PAI-I in plasma from kidney allograft recipients. We studied 64 patients who underwent kidney transplantation from cadaveric allograft donors. At the time of the study 38 patients had stable graft function for at least 6 months proceeding the study, and 26 recipients had biopsy-proven chronic rejection of the kidney transplant. Control group included 30 healthy blood donors. In kidney transplant recipients we found significantly higher plasma tPA activity (median: 0.99 IU/ml; range: 0-3.8 IU/ml) in comparison to healthy controls (median: 0.15 IU/ml; range: 0-2.8 IU/ml) (p = 0.002) as well as significantly lower plasma PAI-I activity (median: 7.06 U/ml; range: 0-33.2 U/ml) in comparison to healthy controls (median: 21.8 U/ml; range: 0-36.7 U/ml), (p = 0.0001). Among transplant recipients, PAI-I plasma activity in recipients with chronic graft rejection (median: 10.16 U/ml; range: 0-33.2 U/ml) was significantly higher than in patients with stable graft function (median: 4.83 U/ml; range: 0-22.9 U/ml), (p = 0.01). In transplant recipients with stable graft function and poorly controlled hypertension we found significantly higher PAI-I plasma activity in comparison to recipients with normal blood pressure (p = 0.006). In kidney transplant recipients there was a positive correlation between the dose of prednisone and PAI-I activity in plasma (p = 0.01) and an association between BMI value and plasma PAI-I activity (p = 0.008), as well as an association between BMI value and plasma tPA-Ant concentration (p = 0.006). Among transplant recipients, patients treated with ACE inhibitors had significantly lower uPA plasma activity than the rest of the group (p = 0.003). In recipients with stable graft function we found a correlation between CsA concentration and tPA activity (p = 0.04), as well as an association between the dose of CsA and uPA-Ant concentration in plasma (p = 0.049). In patients with chronic graft rejection we found a negative correlation between the dose of prednisone and uPA-Ant plasma level (p = 0.004). Renal allograft recipients have higher tPA and lower PAI-I activities in plasma in comparison to healthy individuals. Chronic allograft rejection, is as well as poorly controlled hypertension, seem to be associated with an increase PAI-I plasma activity. In kidney graft recipients there is a relation between the value of BMI and the activity and concentration of tPA-Ant as well as the value of BMI and the PAI-I activity in plasma. Poorly controlled hypertension is associated with an increase in PAI-I plasma activity. The results of our study suggest a stimulatory effect of CsA on tPA and PAI-I plasma activities as well as on uPA-Ant concentration, while prednisone in turn seems to enhance PAI-I activity in plasma and decrease uPA expression. In renal allograft recipients ACE inhibitors seem to reduce uPA plasma activity.
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PMID:The effect of chronic allograft rejection on plasma regulators of fibrinolysis. 1222 3

In Alzheimer's disease (AD) Abeta accumulates because of imbalance between the production of Abeta and its removal from the brain. There is increasing evidence that in most sporadic forms of AD, the accumulation of Abeta is partly, if not in some cases solely, because of defects in its removal--mediated through a combination of diffusion along perivascular extracellular matrix, transport across vessel walls into the blood stream and enzymatic degradation. Multiple enzymes within the central nervous system (CNS) are capable of degrading Abeta. Most are produced by neurons or glia, but some are expressed in the cerebral vasculature, where reduced Abeta-degrading activity may contribute to the development of cerebral amyloid angiopathy (CAA). Neprilysin and insulin-degrading enzyme (IDE), which have been most extensively studied, are expressed both neuronally and within the vasculature. The levels of both of these enzymes are reduced in AD although the correlation with enzyme activity is still not entirely clear. Other enzymes shown capable of degrading Abetain vitro or in animal studies include plasmin; endothelin-converting enzymes ECE-1 and -2; matrix metalloproteinases MMP-2, -3 and -9; and angiotensin-converting enzyme (ACE). The levels of plasmin and plasminogen activators (uPA and tPA) and ECE-2 are reported to be reduced in AD. Reductions in neprilysin, IDE and plasmin in AD have been associated with possession of APOEepsilon4. We found no change in the level or activity of MMP-2, -3 or -9 in AD. The level and activity of ACE are increased, the level being directly related to Abeta plaque load. Up-regulation of some Abeta-degrading enzymes may initially compensate for declining activity of others, but as age, genetic factors and diseases such as hypertension and diabetes diminish the effectiveness of other Abeta-clearance pathways, reductions in the activity of particular Abeta-degrading enzymes may become critical, leading to the development of AD and CAA.
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PMID:Abeta-degrading enzymes in Alzheimer's disease. 1836 35

The endothelium plays a key role in the development of atherogenesis and its inflammatory and proliferative status influences the progression of atherosclerosis. The aim of this study is to compare the effects of two beta blockers such as nebivolol and atenolol on gene expression in human umbilical vein endothelial cells (HUVECs) following an oxidant stimulus. HUVECs were incubated with nebivolol or atenolol (10 micromol/L) for 24 hours and oxidative stress was induced by the addition of oxidized (ox)-LDL. Ox-LDL upregulated adhesion molecules (ICAM-1, ICAM-2, ICAM-3, E-selectin, and P-selectin); proteins linked to inflammation (IL-6 and TNFalpha), thrombotic state (tissue factor, PAI-1 and uPA), hypertension such as endothelin-1 (ET-1), and vascular remodeling such as metalloproteinases (MMP-2, MMP-9) and protease inhibitor (TIMP-1). The exposure of HUVECs to nebivolol, but not to atenolol, reduced these genes upregulated by oxidative stress both in terms of protein and RNA expression. The known antioxidant properties of the third generation beta blocker nebivolol seem to account to the observed differences seen when compared to atenolol and support the specific potential protective role of this beta blocker on the expression of a number of genes involved in the initiation and progression of atherosclerosis.
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PMID:Effects of nebivolol on endothelial gene expression during oxidative stress in human umbilical vein endothelial cells. 1843 28


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