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)

Acute stroke presents an emergency that requires immediate referral to a specialized hospital, preferably with a stroke unit. Disability and mortality are reduced by 30% in patients treated in stroke units compared to those treated on regular wards, even if a specialized team is present on the ward. Systolic blood pressure may remain high at 200-220 mmHg in the acute phase and should not be lowered too quickly. Further guidelines for basic care include: optimal O2 delivery, blood sugar levels below 100-150 mg%, and lowering body temperature below 37.5 degrees C using physical means or drugs. Increased intracranial pressure should be treated by raising the upper body of the patient, administration of glycerol, mannitol, and/or sorbitol, artificial respiration, and special monitoring of Tris buffer. Decompressive craniectomy may be considered in cases of "malignant" media stroke and expansive cerebellar infarction. Fibrinolysis is the most effective stroke treatment and is twice as effective in the treatment of stroke than myocardial infarction. Fibrinolysis may be initiated within 3 h of a stroke in the anterior circulation. If a penumbra is detectable by "PWI-DWI mismatch MRI," specialized hospitals may perform fibrinolysis up to 6 h after symptom onset. In cases of stroke in the basilar artery, fibrinolysis may be performed even later after symptom onset. Intra-arterial fibrinolysis is performed in these cases using rt-PA or urokinase. Follow-up treatment of stroke patients should not only address post-stroke depression and neuropsychological deficits, but also include patient education about risk factors such as high blood pressure, diabetes mellitus, and cardiac arrhythmias.
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PMID:[Basics of acute stroke treatment]. 1586 21

The serine proteases of the trypsin superfamily are versatile enzymes involved in a variety of biological processes. In the cardiovascular system, the importance of these enzymes in blood coagulation, platelet activation, fibrinolysis, and thrombosis has been well established. Recent studies have shown that trypin-like serine proteases are also important in maintaining cardiac function and contribute to heart-related disease processes. In this review, we describe the biological function of corin, tissue kallikrein, chymase and urokinase and discuss their roles in cardiovascular diseases such as hypertension, cardiac hypertrophy, heart failure, and aneurysm.
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PMID:Serine proteases and cardiac function. 1605 20

A 74-year-old man with hypertension and diabetes mellitus was admitted to our hospital because of acute exacerbation of chronic renal failure after treatment with urokinase for a cerebral infarction. A percutaneous renal biopsy was performed to examine the cause of renal damage, revealing glomerulosclerosis and cholesterol clefts in the small arteries. Subsequently eosinophil was increased to 21% and livedo reticularis was found in the patient's foot. A skin biopsy was performed, and cholesterol clefts were again found in the small arteries. For the reason, our diagnosis was cholesterol crystal embolism. Although 30 mg of prednisolone was administered, the patient's renal function did not improve and maintenance hemodialysis therapy was necessary. This is a rare case of cholesterol crystal embolism caused by urokinase without any invasive vascular procedures.
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PMID:[Case of cholesterol crystal embolism occurring after treatment of cerebral infarction with urokinase]. 1677 2

Primary intraventricular haemorrhage (IVH) is rare. We defined primary IVH as haemorrhage into the ventricles only as detected by computerized tomographic (CT) brain scan. This is in contrast with other intracerebral haemorrhages (e.g. basal ganglia/thalamic with intraventricular extension). The clinical condition of the patient ranges from minimal neurological deficits to coma/death. It also carries with it a poor prognosis of up to 80% when all four ventricles are involved. We present a 45-year-old Chinese female who presented with a hypertensive IVH which was managed successfully with ventricular drainage and intraventricular urokinase therapy. An adrenal phaeochromocytoma was diagnosed which was subsequently removed laparoscopically. The patient has recovered well in all aspects. This case report will discuss management of IVH and the importance of searching for secondary causes of hypertension.
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PMID:Hypertensive primary intraventricular hemorrhage due to a phaeochromocytoma. 1681 39

Myofibroblasts are involved in vessel remodeling during the development of hypertension as well as after angioplasty and aortocoronary grafting, but the mechanisms of myofibroblastic phenotypic modulation are not fully elucidated. We assessed the role of urokinase plasminogen activator (uPA) and its proteolytic activity in myofibroblast differentiation and the early proliferation following mechanical injury of the rat carotid adventitia. The effects of perivascular application of recombinant uPA (r-uPA), proteolytically inactive r-uPA(H/Q) and uPA neutralizing antibody were evaluated 4 days after surgical injury to the adventitia. The phenotype of adventitial cells was assessed using anti-alpha-smooth muscle actin (alpha-SM actin) antibody, anti-SM heavy chain myosin, anti-high-molecular-weight caldesmon, anti-smoothelin and anti-ED-1 antibodies, proliferation by the expression of proliferating cell nuclear antigen, and the size of the adventitia by quantitative morphometry. Four days after injury, the intensive immunostaining for urokinase appeared in the rat carotid artery adventitia. At the same time, the frequency of alpha-SM actin-positive adventitial cells was 1.8+/-1.1% in uninjured arteries and 25.2+/-5.4% in injured arteries (p<0.05), and the respective frequency of ED-1-positive cells 1.5+/-1.1 and 25.0+/-5.2%. The application of exogenous r-uPA doubled the numbers of alpha-SM actin-positive adventitial cells to 55.7+/-6.8% (p<0.05). ED-1-positive cells and proliferating cell nuclear antigen-positive cells as well as the size of the adventitia were also significantly increased after r-uPA compared with injury alone. In contrast, the proteolytically inactive r-uPA(H/Q) did not affect any parameters. The application of uPA neutralizing antibody attenuated the frequency of alpha-SM actin-positive cells to 12.6+/-3.5% (p<0.05), the frequency of ED-1-positive cells, and the numbers of adventitial cells. r-uPA stimulation of cultured human skin fibroblasts significantly increased the alpha-SM actin content in a concentration-dependent manner. In contrast, r-uPAH/Q did not induce changes in alpha-SM actin content. We conclude that uPA, which is upregulated in the injured adventitia, can augment adventitial cell accumulation, including myofibroblasts, and adventitia growth early after injury of the rat carotid artery adventitia by mechanisms involving proteolysis.
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PMID:Urokinase plasminogen activator in injured adventitia increases the number of myofibroblasts and augments early proliferation. 1689 94

Given the poor natural history of untreated symptomatic acute middle cerebral artery occlusion, we have attempted emergent reperfusion in all three cases of acute embolic middle cerebral artery occlusion seen on our cranial base service over the last 10 years. One patient developed a massive stroke requiring a life-saving "strokectomy" within 48 hours, which left him permanently hemiplegic, hemianopic, and hemihypesthetic after a failed attempt at reperfusion by superselective endovascular injection of urokinase. The other two patients, who were aphasic and densely hemiparetic, underwent successful emergent embolectomy with reperfusion established within 5 and 12 hours, respectively. One of the two is now neurologically normal, and the second is left with a subtle monoparesis but is independent in activities of daily living. Since middle cerebral artery embolism in cranial base patients usually occurs in a closely monitored hospital setting, we are presented with a unique opportunity for early successful operative intervention. Principles for optimizing outcome include: early recognition and diagnosis, maximization of medical therapy during the diagnostic workup prior to embolectomy (induced hypertension, intravascular volume expansion, and pharmacologic cerebral metabolic demand reduction), confirmation that the involved region does not have absent blood flow by xenon/computed tomography, early operative intervention, and careful surgical technique.
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PMID:Emergent middle cerebral artery embolectomy: a useful technique for cranial base surgery. 1717 Aug 94

Chronic kidney disease (CKD) is common in China. In residents older than 40 years in Beijing, China, 11.3% of subjects had at least one indicator of kidney damage. The primary cause of chronic renal failure in China was glomerulonephritis, which was followed by diabetic nephropathy and hypertensive nephrosclerosis. Renal failure, cardiovascular disease and infection were important complications. IgA nephropathy (IgAN) is the most common CKD in China. The prevalence of hypertension, intrarenal artery lesions and tubulointerstitial lesions in patients with IgAN at the time of renal biopsy was approximately 40, 55 and 85%, respectively. The genetic variation in Megsin confers susceptibility to IgAN in Chinese. The patients with SL/LL genotypes of the MUC20 gene, the 38AA genotype of uteroglobin and DD genotype of the angiotensin-converting enzyme gene had a higher risk of progression. Chinese prospective clinical trials showed that benazepril (BZ) conferred substantial renal benefits in patients with advanced renal insufficiency. The combined therapy with urokinase and BZ was more effective than with BZ alone in reducing proteinuria and protecting renal function in Chinese patients with severe IgAN. Lupus nephritis (LN) is a common form of secondary renal disease diagnosed by renal biopsy in China. Chinese multicenter clinical trials showed that mycophenolate mofetil or leflunomide combined with steroids was effective as induction therapy for proliferative LN.
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PMID:Epidemiology, major outcomes, risk factors, prevention and management of chronic kidney disease in China. 1789 Aug 52

Intraventricular extension of hemorrhage after intraparenchymal hemorrhage is associated with significant morbidity and mortality. Clinical improvement is reported in a patient with thalamic hemorrhage with intraventricular extension after third and fourth ventricular blood clot resolution with instillation of urokinase intraventricularly. A 49-year-old man with hypertension collapsed while at work. A computed tomography (CT) scan of the head revealed a left thalamic hemorrhage with extension into the lateral, third, and fourth ventricles and associated hydrocephalus. A left frontal intraventricular catheter (IVC) was placed and intraventricular urokinase was administered at a dose of 25,000 U every 12 hours. The CT scan revealed resolution of the lateral ventricular dilatation and blood clot but no decrease in third or fourth ventricular hemorrhage. No clinical improvement was noted. The IVC was reinserted on the right side with the catheter tip placed through the foramen of Monroe into the third ventricle. Twelve hours after receiving the first dose of urokinase through the new catheter, the patient's condition improved. The CT scan showed a reduction in the volume of blood of the third and fourth ventricles. This case report shows that treatment of hydrocephalus with an IVC was not sufficient to provide a therapeutic effect. Substantial clinical improvement occurred only after the blood clot was cleared from the third and fourth ventricles.
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PMID:Clinical improvement related to thrombolysis of third ventricular blood clot in a patient with thalamic hemorrhage. 1790 95

Intraventricular haemorrhage (IVH) is associated with a poor outcome. Simple external ventricular drainage has not modified the high morbidity and mortality of these patients. Our objective was to review our experience using intraventricular urokinase (UK) in treating patients with moderate to severe IVH. Prospective analysis of medical records of 14 patients diagnosed with spontaneous IVH who received ventriculostomy and intraventricular infusion of UK from January 2002 to December 2005. Patients with the following characteristics were included: 18-70 years of age, GCS between 5 and 14, and moderate to severe IVH (Graeb > or = 6) without simultaneous intraparenchymal haematoma > 30 ml. The final results were compared to historic control group (14 patients) treated between January 1999 to December 2001 with ventriculostomy alone. All 28 patients accomplished the inclusion criteria. Patient age, initial GCS and Graeb classification of IVH were similar in the two groups of treatment. There was higher ventriculostomy obstruction rate in the non-UK group (33.3 vs. 0%; p > 0.05), a higher rate of intracranial hypertension in the non-UK group (66.6 vs. 16.6%; p = 0.036) and a lower mortality rate in the UK group (25 vs. 58.3%, p > 0.05). There was no rebleeding associated with UK treatment. Intraventricular UK appears to be a safe treatment. It is effective in the prevention of catheter blockage, speeding the clearance of IVH, and it is associated with lower rate of intracranial hypertension and death.
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PMID:Fibrinolytic therapy in spontaneous intraventricular haemorrhage: efficacy and safety of the treatment. 1834 24

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


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