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)

Urapidil (URA) is used to treat acute hypertension in patients with coronary artery disease, but the effect of URA on the performance of ischemic myocardium has not yet been investigated. The present study was intended to assess the function of ischemic myocardium following URA administration. In eight anesthetized (piritramide) open-chest dogs systolic contraction (dL) and end-diastolic length (edL) of myocardium supplied by the left descending (LAD) and circumflex (LCA) coronary arteries were measured by sonomicrometry simultaneously with aortic pressure (AoP), left ventricular end-diastolic pressure (LVedP), heart rate (HR), stroke volume (SV), and LAD-flow (QLAD). QLAD was reduced by LAD stenosis to about 50% of control, decreasing dLLAD by 55%. Concomitantly, edLLAD increased by about 9% and LVedP by 22%, whereas AoP decreased by 5%. Then, URA was given i.v. (0.25 + 0.25 + 0.50 + 1.0 mg/kg) in 15-min intervals. Following URA, the performance of the non-ischemic area was not systematically affected, but dLLAD increased by about 50%. This could neither be related to the significant reduction in afterload (AoP: -8%), nor to an increase in preload (LVedP and edLLAD did not change significantly), nor to an improved oxygen supply via the LAD (QLAD even decreased), although an increased collateral flow the LCA could not be excluded. The increase in systolic shortening correlated very closely to a decrease in heart rate (r = -0.92). It is concluded that the improved function of ischemic myocardium following urapidil resulted from a reduced oxygen demand in consequence to the decrease in heart rate.
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PMID:Effect of urapidil on the performance of ischemic myocardium in anesthetized dogs. 238 20

The effect of urapidil on the ischaemic myocardium was studied in eight anaesthetized dogs. Stenosis of the left descending coronary artery reduced blood flow and systolic contraction of the post-stenotic myocardium by about 50%; the end-diastolic length of the post-stenotic myocardium and the end-diastolic pressure increased, while aortic pressure slightly decreased. Subsequent administration of urapidil (0.25 + 0.25 + 0.5 + 1.0 mg/kg intravenously) did not affect the systolic shortening and end-diastolic length of the myocardium supplied by the left circumflux coronary artery, while the stroke volume and the systolic shortening of the ischaemic myocardium increased. The latter was correlated with a decrease in the heart rate (r = -0.92), but not with the reduction in aortic pressure. Urapidil by itself does not impair the performance of the ischaemic myocardium, but might be beneficial in decreasing the heart rate or suppressing reflex tachycardia during reduction of the afterload.
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PMID:Effect of urapidil on the performance of ischaemic myocardium in anaesthetized dogs. 257 70

The left ventricular hemodynamic changes were studied in 9 hypertensive patients (6 patients with hypertensive attack and 3 patients with a severe form of the disease) by simultaneous recordings of the M-type echocardiogram, apexcardiogram and phonocardiogram in an acute trial with Urapidil administered intravenously in a dose of 0,7 mg/kg body mass. The arterial pressure and the peripheral vascular resistance decrease. The stroke and the minute volume do not change. The heart rate increases. The telediastolic and telesystolic dimensions of the left ventricle decrease. The percentage amplitude of the aI-wave of the apexcardiogram also decreases. The fraction of the shortening of the left ventricular dimension increases with 23,0%, the ejection fraction increases with 13,5% and the average speed of the circumferential fibres shortening increases with 21,4%. Urapidil applied i.v. exerts a rapid hypotensive action and improves the left ventricular function.
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PMID:[Hemodynamic changes and left ventricular function in patients with hypertension during an acute trial of urapidil]. 306 99

To examine the hemodynamic changes induced by vasodilator therapy with urapidil during exercise in patients with chronic obstructive pulmonary disease (COPD) and their potential impact on symptom-limited maximal oxygen consumption, we studied 12 clinically stable patients using a randomized, crossover design. Placebo or urapidil (60 mg orally thrice a day) was given during 48 h preceding each incremental maximal exercise testing. Urapidil compared to placebo consistently lowered the pulmonary artery pressure either at rest from 29 +/- 2.5 to 24 +/- 1.5 mm Hg (p less than 0.001) or during exercise from 55 +/- 3 to 46 +/- 2 mm Hg (p less than 0.01). At rest, the systemic arterial pressure was reduced from 97.5 +/- 4 to 88.5 +/- 3 mm Hg (p less than 0.001) with no significant difference in heart rate or cardiac index. During exercise, systemic arterial pressure decreased from 135 +/- 4 to 119 +/- 3 mm Hg (p less than 0.001). As compared to placebo, urapidil tended to increase the cardiac index from 6.1 +/- 0.4 to 6.6 +/- 0.4 L/min.m2 (NS) and to decrease heart rate, from 122 to 116 beats/min (NS); the resulting stroke volume index increased with urapidil from 49 +/- 3 to 57 +/- 4 ml/m2 (p less than 0.01); at rest, urapidil did not induce alteration in gas exchange, while during exercise, C(a-v)O2 decreased from 8.6 +/- 0.5 to 7.7 +/- 0.4 vol% (p less than 0.01), SVO2 increased from 39.5 +/- 2 to 44.5 +/- 1.5% (p less than 0.01), and SaO2 from 82 +/- 2 to 85 +/- 2% (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of urapidil therapy on hemodynamics and gas exchange in exercising patients with chronic obstructive pulmonary disease and pulmonary hypertension. 314 77

To test the hypothesis that the hypotensive action of urapidil is in part related to a direct action on the brain, the central (intracerebroventricular) and peripheral (intravenous) effects of urapidil were studied and compared with those obtained with clonidine and prazosin. All studies were conducted in conscious, chronically instrumented stroke-prone spontaneously hypertensive rats (SHRSP). Efferent sympathetic nervous system activity was estimated by means of a bipolar electrode implanted on the splanchnic nerve. Only clonidine, administered intracerebroventricularly and intravenously, decreased sympathetic nerve activity. Urapidil and prazosin either did not affect sympathetic nerve activity after central administration or increased it after peripheral administration at low and high doses, respectively. Centrally administered urapidil and prazosin lowered blood pressure but also blocked the response to intravenously administered phenylephrine; this result suggests a peripheral effect. Centrally administered urapidil decreased heart rate. Urapidil given either intracerebroventricularly or into the cisterna magna had no influence on baroreceptor responses. Intravenous infusions of urapidil and prazosin in sufficient doses to lower blood pressure in spontaneously hypertensive rats by 50 mm Hg completely blocked the actions of phenylephrine. These data suggest that in conscious SHRSP urapidil lowers blood pressure through peripheral blockade of alpha 1-adrenergic receptors rather than by means of central sympathetic suppression. In this regard urapidil resembles prazosin rather than clonidine; however, the effect of urapidil on heart rate is consistent with a central mode of action.
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PMID:Effect of urapidil, clonidine, and prazosin on sympathetic tone in conscious rats. 395 16

We have studied the effects of urapidil 0.4 mg kg-1 i.v. and clonidine 2.5 micrograms kg-1 i.v. on left ventricular volume and function in 20 patients with chronic coronary artery disease and essential hypertension. Patients were studied using 99mtechnetium radionuclide angiography with first-pass and ECG-gated equilibrium blood-pool techniques and non-invasive sphygmomanometry. Administration of both urapidil and clonidine caused a similar decrease in mean arterial pressure (20%), associated with an equivalent reduction in systemic vascular resistance. Despite the decrease in mean arterial pressure, heart rate did not change after administration of clonidine, but there was an early and transient increase of 13% after urapidil. There were no changes in cardiac index, but in contrast with clonidine, urapidil caused a decrease in stroke index. In both groups, global left ventricular ejection fraction did not change. Urapidil produced a mean decrease in end-diastolic volume of 8% and a mean decrease in end-systolic volume of 13%, in contrast with clonidine which caused little change. Reduced arterial pressure, systemic vascular resistance and preload after urapidil 0.4 mg kg-1 i.v., associated with lack of prolonged tachycardia and preserved global left ventricular performance, may have obvious clinical implications in anaesthesia.
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PMID:Acute effects of urapidil on left ventricular function in hypertensive patients: comparison with clonidine using radionuclide angiography. 791 46

Stroke is a partly preventable neurological disease associated with excessive economic cost. Adequate prevention of stroke and sufficient therapy in the acute phase will help to reduce the heavy burden of morbidity and severe economic impact. Hypertension as such, and even more so stroke itself, are known to influence cerebral autoregulation in a negative sense. With respect to the prevention of stroke, antihypertensive therapy should be accompanied by attempts to inhibit of atherogenesis, for instance via improvements of the lipid profile (lowering of LDL, elevation of HDL) or via inhibition of platelet aggregation. In conditions of acute stroke, a pharmacologically induced rise in intracranial pressure should be avoided, whereas cerebral perfusion pressure must be maintained. If possible, ischaemic tolerance should be increased. Also with respect to the secondary prevention of stroke, antihypertensive therapy should be aiming at maintaining cerebral blood flow, whereas the progression of atherosclerotic lesions should be impaired as much as possible. Urapidil may be characterised as a peripheral alpha 1-adrenoceptor blocker with additional sympathoinhibitory effect, triggered by the stimulation of central 5HT1A-receptors. Urapidil, well documented as an effective antihypertensive agent in short- and long-term trials, also showed beneficial influence in the acute phase of stroke. After 3 years of treatment with urapidil (60 mg b.i.d.), the total cardiovascular risk proved reduced by 26%. In addition, urapidil influenced lipid profile, glucose metabolism, and platelet aggregation favourably in hypertensive patients. In animal experiments, urapidil improved the ischaemic tolerance of the brain. Taken together it would seem worthwhile to investigate urapidil as a possibly beneficial agent in the treatment of acute stroke, as well as in secondary prevention of this condition.
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PMID:Potential beneficial effects of urapidil in primary and secondary prevention of stroke. 853 45

Hypertensive crises are situations when arterial hypertension shows its immediate damaging potential, and in such circumstance, antihypertensive therapy provides its life-saving effectiveness. Among these situations are hypertensive emergencies, hypertensive urgencies, hypertensive encephalopathy, and also accelerated-malignant hypertension characterised by the presence of grade 3 or grade 4 Keith-Wagener retinopathy and numerous complications (acute renal failure, heart failure, haemorrhagic brain stroke or acute coronary events). Despite of antihypertensive therapy, the mortality rate of accelerated-malignant hypertension is about 25% after the 5th year. We present the case of a thirty-three years old male, with a five-year history of non-treated hypertension, who develops accelerated- hypertension with heart failure, microangiopathic haemolytic anaemia and renal failure that requires renal replacement therapy. After a strict control of blood pressure; initially using parenteral agents such as Solinitrin and Urapidil, followed by angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, beta-adrenergic receptor blockers, calcium channel blockers and Hydralazine, the patient partially recovers his renal function, resulting in the withdrawal of haemodialysis.
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PMID:[Accelerated arterial hypertension in a young male]. 1521 76

Despite the availability of a wide range of effective blood pressure (BP)-lowering agents, a substantial proportion of patients with hypertension fail to achieve target BP levels. The majority of patients with hypertension need a combination of two or more drugs to achieve BP targets and choice of second-line or subsequent-line therapy is an important consideration in hypertension management. Alpha-1-adrenoreceptor antagonists (alpha-blockers) have a BP-lowering effect broadly similar to the other antihypertensive drug classes and are effective as add-on therapy in patients with inadequately controlled hypertension. Alpha-blockers may also have therapeutic benefits that go beyond BP control, including improvements in lipid profile and glucose metabolism, as well as reducing the symptoms of benign prostatic hyperplasia. Urapidil has an alpha-blocking effect but, unlike other alpha-blockers, also has a central sympatholytic effect mediated via stimulation of serotonin 5HT(1A) receptors in the central nervous system. Several studies have suggested that oral urapidil is effective and well tolerated when used as second-line therapy in patients with BP inadequately controlled with other agents. Urapidil has also been shown to improve glucose and lipid metabolism in hypertensive patients with concomitant diabetes and/or hyperlipidemia. Intravenous urapidil is effective in the treatment of hypertensive crises, perioperative hypertension, and pre-eclampsia and may have a potential role in the management of acute stroke. In this review, the use of alpha-blockers in hypertension is discussed, with particular focus on urapidil for the lowering of BP in a variety of clinical settings.
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PMID:Urapidil, a dual-acting antihypertensive agent: Current usage considerations. 2065 59