Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atrial natriuretic peptide (ANP) is a cardiac hormone which affects endothelial cell function through a receptor-mediated process. Pneumonectomy is a common thoracic surgical procedure that can cause pulmonary oedema in the remaining lung. Few reports have investigated the aetiology of this complication. The aim of this study was to determine the changes in ANP concentration and expression of its receptors following pneumonectomy as a possible aetiology for postpneumonectomy pulmonary oedema (PPE). We compared plasma ANP concentrations, cGMP concentrations, and natriuretic peptide receptor (NPR)-A mRNA and NPR-C mRNA expression in rat lung 3 h after pneumonectomy (n=5) or a sham operation (n=5). The ANP concentrations in plasma and lung tissue in the pneumonectomy group were significantly higher than in the control group (749.5 versus 202.7 pg x ml(-1), P<0.01; 33.1 versus 6.8 ng x g(-1) wet tissue, P<0.01 respectively). The level of ANP mRNA expression in the pneumonectomy group was significantly higher than in the control group (1.44 versus 0.41 relative ANP mRNA expression, P<0.05). The concentration of cGMP and the level of NPR-A mRNA expression were not significantly different between the pneumonectomy and control groups. The level of NPR-C mRNA expression in the pneumonectomy group was significantly higher than in the control group (4.17 versus 2.19 relative NPR-C mRNA expression, P<0.01). These findings suggest that changes in pulmonary ANP and NPR-C expression may contribute to the development of PPE in the remaining lung in the acute phase following pneumonectomy.
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PMID:Changes in atrial natriuretic peptide concentration and expression of its receptors after pneumonectomy in the rat. 1099 1

We evaluated the effects of human natriuretic peptide (hANP) on the recipients of living-related renal transplantation in children. Anesthesia was maintained with nitrous-oxide and isoflurane in oxygen. The recipients were divided into two groups: the hANP group (n = 8) received continuous infusion of hANP (0.1 microgram.kg-1.min-1), and the control group (n = 5) received no hANP infusion. Intravenous hANP infusion was started at the loading time of fresh frozen plasma in the recipients until the 12 hours after operation. There were no differences between the groups with regards to age, height, body weight, changes in heart rate and systolic arterial pressure, urine volume during operation, and the levels of blood uremic nitrogen and creatinine. The hANP group showed minimal change in CVP during operation and body weight between the values during and after operation compared with control group. The control group needed significantly more fluid than hANP group during operation. We concluded that continuous i.v. hANP infusion in the pediatric recipients of living-related renal transplantation was useful for maintaining sufficient urination and prevention of heart failure or lung edema.
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PMID:[The effects of human atrial natriuretic peptide on the pediatric recipients of living-related renal transplantation]. 1107 61

Although the dehydration-rehydration problem in end-of-life care is one of the most important issues, clinical indications of hydration therapy have not been clarified because the pathophysiology is poorly understood. To explore the physiological changes of fluid status in terminally ill cancer patients, a prospective observational study was performed. We obtained 9 pairs of blood samplings from hospice inpatients with irreversible bowel obstruction who underwent two or more laboratory examinations during the admission periods. The plasma renin activity (PRA) and brain natriuretic peptide (BNP) were measured, in addition to basic laboratory tests performed as clinically required. A chart review evaluated the degree of fluid retention symptoms. In 7 patients receiving intravenous rehydration of 700-2200 ml/day, the mean PRA level significantly increased from 3.5+/-2.5 ng ml(-1) h(-1) to 11+/-8.2 ng ml(-1) x h(-1) ( P=0.047), and the mean BNP level significantly decreased from 52+/-34 pg/ml to 22+/-14 pg/ml ( P=0.047). Edema, ascites, and pleural effusion/pulmonary edema deteriorated in 5, 3, and 5 patients, respectively. In 2 patients without rehydration therapy, peripheral edema deteriorated with increased PRA levels (0.5 to 20 ng ml(-1) x h(-1), 0.4 to 8.7 ng ml(-1) x h(-1), respectively). In conclusion, intravenous volume depletion with fluid retention symptoms was observed in terminally ill cancer patients with intestinal obstruction both receiving and not receiving intravenous hydration. The pathological mechanism hypothesized is the fluid shift from the intravascular compartment to the interstitial spaces.
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PMID:Fluid status of terminally ill cancer patients with intestinal obstruction: an exploratory observational study. 1235 26

Patients with acute congestive heart failure generally present with profound fluid retention states and dyspnea due to pulmonary edema. If the condition is not aggressively and appropriately treated, irreversible cardiac decompensation may ensue, leading to cardiogenic shock, multiorgan failure, and death. Intravenous inotropic, vasopressor, and vasodilator therapies have proved effective in initial stabilization of acute heart failure decompensation, but these agents, particularly the traditionally used ones, are generally limited by side effects that can be egregious and include substantive ventricular arrhythmias. Dobutamine has largely replaced agents with rather profound toxicity, such as isoproterenol and epinephrine. The phosphodiesterase-inhibiting agent milrinone, having both vasodilator and inotropic properties, can produce tachycardia and significant ventricular arrhythmias, but has proven quite useful for seriously ill patients. Clinical trials of levosimendan have found a positive inotropic response when the drug is given parenterally; vasodilating properties are also evident. Clinical trials are under way to evaluate the potential benefits of endothelin receptor antagonists when given intravenously. Intravenous administration of nesiritide, a recombinant human B-type natriuretic peptide, has been shown to produce favorable hemodynamic effects, including balanced vasodilation associated with a rapid improvement in clinical symptoms.
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PMID:New therapeutic choices in the management of acute congestive heart failure. 1243 58

The standard treatment for acute heart failure (synonymous with pulmonary edema) is an upright posture, oxygen, morphine (often accompanied by an antiemetic), and intravenous diuretics. This treatment has remained unchanged for many years, and the precise mechanism by which each of these methods alleviates symptoms in patients is unclear. Nitrates, oral or intravenous, are also used with benefit, and have some hemodynamic advantages over intravenous diuretics. Recently, three new forms of treatment have been investigated. The use of milrinone, a phosphodiesterase inhibitor, for exacerbation of heart failure in patients with a background of chronic heart failure was not advantageous. The trials of levosimendan, a calcium sensitizer, in patients with pulmonary edema hinted at benefit. Nesiritide, a formulation of brain natriuretic peptide, does bring about hemodynamic improvement in acute heart failure, and is at least as effective as nitroglycerin, easier to prescribe, but prone to cause hypotension. These are small but important advances that increase our knowledge of the pathophysiology of acute heart failure, and also provide an indication of which drugs are preferable for the treatment of this distressing condition.
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PMID:New therapies for the management of acute heart failure. 1269 42

MODALITIES FOR THE DIAGNOSIS OF VENOUS THROMBOEMBOLISM: Currently rely on the confrontation of the initial clinical data and the results of D-dimer measurements, a venous Doppler, although reliable, is not a first-line exploration. REGARDING TREATMENT: Indications for thrombolysis are currently limited to massive pulmonary oedema with shock. Alteplase added to heparin improves the progression of severe embolism; it spares the patients from heavy interventions of resuscitation but the mortality remains the same. Concerning anticoagulant treatments, prolonged antivitamin K at classical doses is more effective than low doses and for limited duration if phlebitis is an idiopathic one. FOR HEART FAILURE WITH PRESERVED EJECTION FRACTION: Treatment of these heart failures, formerly know as 'diastolic' is similar to that of the acute phase of systolic heart failure. However, care should be taken with vasodilatators. CONCERNING HEART FAILURE IN GENERAL: The brain natriuretic peptide (BNP) represents a remarkable progress for the aetiological diagnosis of dyspnoea (inferior to 80 pg/ml in the case of pulmonary origin, superior to 300 pg/ml in the case of cardiac origin or severe pulmonary embolism). Regarding treatment, for acute heart failure, it is still the association of nitrates and diuretics, with oxygen therapy and eventually inotropics. Beta-blockers, which have revolutionized the treatment of chronic heart failure, must be maintained whenever possible in the case of the onset of acute pulmonary oedema. Multisite pacing is increasingly used in refractory chronic heart failure. Implantable defibrillation has become common practice. Non-invasive ventilation (Bi or C-PAP) is interesting in acute cardiogenic pulmonary oedema. THE PREVENTIVE ROLE OF N ACETYL-CYSTEINE: N acetyl cysteine reduces the incidence of nephropathies induced by the radio contrast products in patients with chronic kidney failure. Combined with hydratation, it must be proposed the day before and on the day of the procedure in any patient with diabetes or kidney failure.
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PMID:[Diagnostic and therapeutic progress. Venous thromboembolism, cardiac insufficiency and radio contrast agents]. 1522 98

We report two cases of neurogenic pulmonary oedema following subarachnoid haemorrhage. A 58-year-old woman became increasingly dyspneic and needed oxygen support during a few days. A 53-year-old woman rapidly developed clinical and laboratory signs of respiratory failure, recovering in 48 hours. In both cases, chest radiography showed bilateral diffuse infiltrates, electrocardiogram revealed ST abnormalities, and cardiac troponin I level was elevated. In both patients, pro brain natriuretic peptide level was increased whereas global cardiac function was normal. The factors initiating its secretion are discussed.
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PMID:[Contribution of the brain natriuretic peptide in neurogenic pulmonary oedema following subarachnoid haemorrhage]. 1558 23

Acute heart failure has recently become a very common syndrome. Therefore, even if you are not a cardiologist, you should know how to diagnose and treat it. A basic technique is here summarized. Diagnosis of heart failure can be performed from a simple criteria including coarse crackles, an extra-sound (S3), a distention of the cervical vein, cardiomegaly, pulmonary edema, and serum levels of B-type natriuretic peptide (100 pg/ml<). After diagnosis, the severity should be assessed by the degrees of both pulmonary edema and cardiac output. For these evaluations, a Swan-Ganz catheter might not be needed, since we can evaluate them clinically, i.e., physical examinations and auscultation. We can then treat the patient with heart failure with a vasodilator and/or diuretics. If the blood pressure is low, we can administer a low dose of an inotropic agent. But an inotropic agent should be withdrawn as early as possible, because they can occasionally have deleterious effects. Finally, please bear in mind that the elimination of several triggers, e.g., infection, transient cessation of medication, and physical or metal stress, and also the detection of early symptoms of heart failure, e.g., shortness of breath on exertion, fatigue, increase in body weight, and appetite loss, are very important for the prevention of acute heart failure.
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PMID:[Diagnostic and therapeutic technique for acute heart failure]. 1567 66

An update is given of the circulating markers and mediators of cardiovascular dysfunction in acute illness. Some of these circulating markers reflect mediator action on the peripheral vasculature, such as endothelium-derived endothelin and nitrite/nitritate, the stable end products of nitric oxide. Other markers mainly reflect actions on the heart, such as the natriuretic peptide family, released from the heart upon dilatation, serving as a marker of congestive heart failure and potentially having negative inotropic effects. Indeed, some factors may be both markers as well as mediators of cardiovascular dysfunction of the acutely ill and bear prognostic significance. Assessing circulating levels may help refine clinical judgment of the cardiovascular derangements encountered at the bedside, together with clinical signs and hemodynamic variables. For instance, assessing natriuretic peptides in patients with pulmonary edema of unclear origin may help to diagnose congestive heart failure and cardiogenic pulmonary edema, when the pulmonary capillary wedge pressure is not measured or inconclusive. Future aligning of hemodynamic abnormalities with patterns of circulating cardiovascular markers/mediators may help to stratify patients for inclusion in studies to assess the causes, response to therapy and prognosis of cardiovascular derangements in the acutely ill.
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PMID:Circulating cardiovascular markers and mediators in acute illness: an update. 1574 96

Beta-adrenergic receptors (betaAR) regulate active Na+ transport in the alveolar epithelium and accelerate clearance of excess airspace fluid. Accumulating data indicates that the cystic fibrosis transmembrane conductance regulator (CFTR) is important for upregulation of the active ion transport that is needed to maintain alveolar fluid homeostasis during pulmonary edema. We hypothesized that betaAR regulation of alveolar active transport may be mediated via a CFTR dependent pathway. To test this hypothesis we used a recombinant adenovirus that expresses a human CFTR cDNA (adCFTR) to increase CFTR function in the alveolar epithelium of normal rats and mice. Alveolar fluid clearance (AFC), an index of alveolar active Na+ transport, was 92% greater in CFTR overexpressing lungs than controls. Addition of the Cl- channel blockers NPPB, glibenclamide, or bumetanide and experiments using Cl- free alveolar instillate solutions indicate that the accelerated AFC in this model is due to increased Cl- channel function. Conversely, CFTR overexpression in mice with no beta1- or beta2-adrenergic receptors had no effect on AFC. Overexpression of a human beta2AR in the alveolar epithelium significantly increased AFC in normal mice but had no effect in mice with a non-functional human CFTR gene (Deltaphi508 mutation). These studies indicate that upregulation of alveolar CFTR function speeds clearance of excess fluid from the airspace and that CFTRs effect on active Na+ transport requires the betaAR. These studies reveal a previously undetected interdependency between CFTR and betaAR that is essential for upregulation of active Na+ transport and fluid clearance in the alveolus.
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PMID:Interdependency of beta-adrenergic receptors and CFTR in regulation of alveolar active Na+ transport. 1580 12


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