Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute heart failure (AHF) is a major cause of hospitalizations. Severe dyspnea, pulmonary congestion and low cardiac output with peripheral vasoconstriction and renal hypoperfusion is a main form of clinical presentation. Most patients with acute worsening have a pre-existing decompensated chronic heart failure (ADCHF), but AHF may also occur as a first manifestation of a previously unknown heart disease. Myocardial ischemia, cardiac arrhythmias, non-compliance with medication and infections are frequent precipitating factors. Management of AHF depends on the underlying heart disease and cause of decompensation. In patients with ADCHF vasodilators and iv diuretics are first-line drugs for rapid reduction of dyspnea and congestion. In patients with signs of low cardiac output and oliguria, inotropic agents are also often administered to prevent further deterioration. Beta-adrenergic agents and phosphodiesterase inhibitors correct the hemodynamic disturbance, but may also induce arrhythmias and worsen myocardial ischemia. Inotropic therapy therefore remains controversial. A novel class of drugs, the calcium sensitizers, represent a new therapeutic option. Levosimendan was shown to improve myocardial contractility without increasing oxygen requirements and to produce peripheral and coronary vasodilation. Its therapeutic effects and tolerance have been tested in several trials. The present review focuses on the clinical pharmacology and therapeutic utility of levosimendan in patients with ADCHF.
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PMID:Newer treatments for decompensated heart failure: focus on levosimendan. 1992 Sep 23

It has been proposed that vasodilatory therapy may increase microcirculatory blood flow and improve tissue oxygenation in septic shock. The authors aimed to evaluate the effects of levosimendan in systemic and splanchnic hemodynamics in a porcine model of septic shock in a randomized animal controlled study. This study was performed in an animal research facility in a university hospital. Anesthetized pigs were monitored with a pulmonary artery catheter and an ultrasonic blood flow probe in the portal vein for measurement of systemic and portal blood flows and with a tonometer placed in the small intestine for measurement of the intramucosal-arterial PCO2 gap. Three groups of pigs were studied: nonseptic (n = 7), septic (n = 7), and septic treated with levosimendan (n = 7). Levosimendan was administered i.v. at t = -10 min (200 microg/kg in i.v. bolus followed by 200 microg/kg per h). Sepsis was induced at t = 0 min by the administration of live Escherichia coli. Vascular reactivity was tested by the hemodynamic response to noradrenaline. Levosimendan markedly attenuated the sepsis-induced increase in pulmonary vascular resistance, decrease in portal/systemic blood flow, oliguria, impairment in oxygenation, hyperkalemia, and the widened intramucosal-arterial PCO2 gap. Systemic blood pressure and vascular resistance did not differ as compared with the septic untreated group. Responses to noradrenaline significantly improved in animals treated with levosimendan. Treatment with levosimendan in this animal model of sepsis attenuated pulmonary vasoconstriction and improved portal blood flow, intestinal mucosal oxygenation, pulmonary function, and vascular reactivity.
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PMID:Levosimendan increases portal blood flow and attenuates intestinal intramucosal acidosis in experimental septic shock. 1999 54