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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of the renal pressure natriuresis and diuresis mechanisms in long-term control of body fluid volumes and arterial pressure has been controversial and difficult to quantitate experimentally. Recent studies, however, have demonstrated that in several forms of chronic hypertension caused by aldosterone, angiotensin II (AngII), vasopressin, or norepinephrine and adrenocorticotropin, increased renal arterial pressure is essential for maintaining normal excretion of sodium and water in the face of reduced renal excretory capability. When renal arterial pressure was servo-controlled in these models of hypertension, sodium and water retention continued unabated, causing ascites, pulmonary edema, or even complete circulatory collapse within a few days. Apparently, other mechanisms for volume homeostasis, such as the various natriuretic and diuretic factors that have been postulated, are not sufficiently powerful to maintain fluid balance in the absence of increased renal arterial pressure when renal excretory function is reduced in these forms of hypertension. The intrarenal mechanisms responsible for pressure natriuresis and diuresis are not entirely clear, but they seem to involve small increases in glomerular filtration rate and filtered load as well as reductions in fractional reabsorption in proximal and distal tubules. During chronic disturbances of arterial pressure additional factors, especially changes in AngII and aldosterone formation, act to amplify the effectiveness of the basic renal pressure natriuresis and diuresis mechanisms in regulating arterial pressure and body fluid volumes.
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PMID:Regulation of arterial pressure: role of pressure natriuresis and diuresis. 353 87

We investigated whether ethchlorvynol (ECV)-induced acute lung injury (ALI) is associated with an increase in leukotriene C4 (LTC4) production. In six pentobarbital sodium-anesthetized dogs, ECV (15 mg/kg iv) introduced into the pulmonary circulation resulted in a 164 +/- 31% increase in extravascular lung water 120 min after ECV administration. Concomitantly, the mean (+/- SE) concentration of LTC4 in arterial plasma measured by radioimmunoassay following 80% EtOH precipitation, XAD-7 extraction and high-pressure liquid chromatography purification was 5.0 +/- 1.3 pg/ml, unchanged from control (pre-ECV) values. In contrast, in pulmonary edema fluid 120 min post-ECV, the LTC4 concentration was 35.2 +/- 10.8 pg/ml, sevenfold greater than those values found in the arterial plasma (P less than 0.01). In six additional dogs, 120 min after unilateral ALI had been induced with ECV (9 mg/kg iv), LTC4 in the bronchoalveolar lavage (BAL) of the uninjured lung was 12.1 +/- 1.5 pg/ml, unchanged from pre-ECV values, whereas, LTC4 in the BAL of the injured lung increased from a control value of 10.2 +/- 1.6 to 24.2 +/- 3.5 pg/ml (P less than 0.01) 120 min after ECV administration. These results demonstrate that, in ECV-induced acute lung injury, LTC4 concentrations in pulmonary edema fluid are considerably greater than those found in arterial plasma in the case of bilateral acute lung injury and significantly greater in the BAL of the injured lung compared with the uninjured lung in the case of unilateral acute lung injury. The results are a necessary first step in support of the hypothesis that leukotrienes participate in the altered permeability of ECV-induced acute lung injury.
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PMID:Increased leukotriene C4 in ethchlorvynol-induced acute lung injury in dogs. 355 33

We have previously presented evidence that cultured alveolar epithelial cell monolayers actively transport sodium from medium to substratum, a process that can be inhibited by sodium transport blockers and stimulated by beta-agonists. In this study, the isolated perfused rat lung was utilized in order to investigate the presence of active sodium transport by intact adult mammalian alveolar epithelium. Radioactive tracers (22Na and [14C]sucrose) were instilled into the airways of isolated Ringer-perfused rat lungs whose weight was continuously monitored. The appearance of isotopes in the recirculated perfusate was measured, and fluxes and apparent permeability-surface area products were determined. A pharmacological agent (amiloride, ouabain, or terbutaline) was added to the perfusate during each experiment after a suitable control period. Amiloride and ouabain resulted in decreased 22Na fluxes and a faster rate of lung weight gain. Terbutaline resulted in increased 22Na flux and a more rapid rate of lung weight loss. [14C]sucrose fluxes were unchanged by the presence of these pharmacological agents. These data are most consistent with the presence of a regulable active component of sodium transport across intact mammalian alveolar epithelium that leads to removal of sodium from the alveolar space, with anions and water following passively. Regulation of the rate of sodium and fluid removal from the alveolar space may play an important role in the prevention and/or resolution of alveolar pulmonary edema.
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PMID:Evidence for active sodium transport across alveolar epithelium of isolated rat lung. 361 Sep 39

A 27-year old female was discovered at 4 a.m. lying in a wet field, the ambient temperature being of 4 degrees C. Her rectal temperature had fallen to 19 degrees C. She was comatose and failed to respond to noxious stimuli. Her pupils were dilated and fixed. Her respiratory rate was reduced to three to four breaths per min. Her blood pressure was not measurable and neither femoral or carotid pulse could be detected. The heart was in sinus rhythm with a rate of 40 b X min-1. During her transfer to hospital, she was ventilated with oxygen, a tidal volume of 300 ml and a rate of 10 b X min-1. On arrival in the emergency room, a short period of ventricular fibrillation preceded cardiac arrest. Cardiac massage and sodium bicarbonate infusion were continued during the transfer of the patient to the operating theatre. A femoro-femoral cardiopulmonary bypass was started with a bloodless priming, 3 mg X kg-1 heparin and a flow of 3,000 to 3,500 ml X min-1. Mean arterial pressure was maintained between 65 and 85 mmHg; cardiac massage was discontinued during the bypass. Within 50 min, ventricular fibrillation appeared, rectal temperature had increased to 33 degrees C. Electrical defibrillation (300 J) was successful. Cardiopulmonary bypass was stopped after 63 min. The postoperative course was uneventful, apart from transient pulmonary oedema. At the time of discharge, a week later, no loss of intellect or change in behaviour could be perceived.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Accidental deep hypothermia and circulatory arrest. Treatment with extracorporeal circulation]. 361 58

A quasi steady-state noninvasive, radioisotopic technique for measuring regional lung water distribution in man is described. The method depends upon the dilution principle. 123I labelled human serum albumin (HSA) and sodium iodide (NaI) were injected intravenously, allowed to mix completely within the body fluids and then counted externally over the chest. The size of each compartment to which the markers are confined was calculated from the external count rate and the isotopic concentration of the marker in plasma. 123I-HSA was used to estimate intravascular water and 123I-NaI extracellular water. Ratio analysis of the differential attenuation of the two photoenergies of 123Iodine (29 keV, 159 keV) by the lung and chest wall was used to estimate the absolute amount of isotope in the lung, independent of chest wall contribution, after validation by phantom studies. Regional pulmonary plasma (PPVr) and interstitial (PIVr) fluid volumes in normal subjects were 7.1 +/- 1.4 and 7.6 +/- 1.3 ml.100 cm-3 lung (mean +/- SD; n = 13) at mid-tidal volume, respectively. In patients with the adult respiratory distress syndrome, PPVr and PIVr were 7.0 +/- 2.9 and 15.9 +/- 4.6 ml.100 cm-3 lung (n = 18), respectively. The pulmonary artery wedge (Paw) pressure was normal (12.5 +/- 2.5 mmHg; n = 5). In patients with pulmonary oedema due to left heart disease, PPVr and PIVr were 7.2 +/- 2.7 and 12.1 +/- 3.7 ml.100 cm-3 lung (n = 8), respectively. The mean Paw pressure in this group was high (28.5 +/- 3.9 mmHg).
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PMID:Noninvasive measurement of regional lung water distribution in healthy man and in pulmonary oedema. 369 23

The side effects of a beta 2-mimetic tocolytic therapy are of importance for anaesthesiologists who administer anaesthesia for obstetric operations, as our case report illustrates. In a healthy 28 year old pregnant woman during the 32nd week of pregnancy i.v. fenoterol was started because of premature labor. After two days severe respiratory failure developed and cesarean section was performed. The patient needed mechanical ventilation with positive endexpiratory pressure and high inspiratory oxygen concentrations (F1O2 greater than 0.7) for 5 days thereafter. The chest x-ray revealed a fluid lung. With artificial respiration and a consequent diuretic therapy with dopamine and furosemide (10 mg . h-1 continuously, negative water balance--5,000 ml on the 4th day) gas exchange improved and extubation was possible on the 6th postoperative day. After exclusion of cardiac or renal disease as well as aspiration of gastric content, the diagnosis of a fenoterol-associated pulmonary edema was thought probable. From the literature it is known that beta 2-mimetics can aggravate the increased water and sodium retention during pregnancy and cause pulmonary edema by an additional increase in pulmonary artery pressure. Therapy consists of adequate oxygenation and induction of diuresis with continuous furosemide and dopamine to achieve negative water balance. When administering anaesthesia to patients on tocolytic therapy positive water balance has to be avoided and great care must be directed to the postoperative gas exchange.
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PMID:[Fenoterol (Partusisten)-associated lung edema. A case report]. 371 43

A fatal case of sodium azide poisoning in which exchange blood transfusions, charcoal hemoperfusion, hemodialysis and potent vasopressor agents failed to prevent the development of circulatory collapse associated with a wide complex cardiac rhythm is presented. The cellular toxin sodium azide resulted in the development of an altered mental status, profound metabolic acidosis, cardiac arrhythmia (atrial fibrillation and terminal wide complex arrhythmias), a relative decrease in cardiac output, hypotension and non-cardiogenic pulmonary edema. Further animal studies are needed to gain new approaches for the treatment of this rare cause of human poisoning.
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PMID:A case of fatal sodium azide ingestion. 374 89

A case is reported of cardiac failure with repeated pulmonary oedema in a female patient suffering from renal failure and having been given incremental doses of dantrolene sodium. On withdrawal of the drug, all symptoms disappeared. This muscle relaxant was considered not to have any depressive myocardial side-effects. However, recent studies on isolated myocardial fibres showed the existence of a constant dose-dependent negative inotropic effect of dantrolene sodium, only noticeable with high concentrations of the drug.
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PMID:[Cardiac failure caused by an overdose of dantrolene]. 382 97

Adult respiratory distress syndrome has been reported after endoscopic variceal sclerotherapy with sodium morrhuate. It has been proposed that sclerosant entering the pulmonary circulation during intravariceal injections may cause pulmonary hypertension and capillary injury. The purpose of this study was to determine whether variceal sclerotherapy with sodium morrhuate causes capillary injury or pulmonary edema in humans. We studied the effect of sclerotherapy on gas exchange and pulmonary and systemic hemodynamics in 8 patients who required endoscopic variceal sclerotherapy for treatment of variceal hemorrhage. The pulmonary vascular resistance index increased from 246 +/- 67 dyn X s X cm-5/m2 (mean +/- SEM) at baseline to a high of 303 +/- 85 dyn X s X cm-5/m2 60 min after sclerotherapy (normal range 250-500 dyn X s X cm-5/m2). Pulmonary artery pressure remained stable while cardiac index decreased by 12% over the same period. There were also small increases in systemic vascular resistance index and systemic arterial pressure after sclerotherapy. Although there was no change in arterial oxygen tension, the alveolar-arterial oxygen difference improved after sclerotherapy. These results indicate that variceal sclerotherapy with sodium morrhuate is associated with clinically insignificant changes in pulmonary and systemic hemodynamics. We did not detect evidence of acute lung injury after sclerotherapy.
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PMID:Effect of endoscopic variceal sclerotherapy on gas exchange and hemodynamics in humans. 387 11

In low-pressure pulmonary edema increased cardiac output (QT) increases shunt (Qs/QT); we tested whether the mechanism is an increase in extravascular lung water in turn mediated by the accompanying increase in microvascular pressure. In six pentobarbital sodium-anesthetized dogs ventilated with O2 we administered oleic acid into the right atrium. From base line to 2 h post-oleic acid we measured concurrent significant increases in Qs/QT (6-29%, O2 technique) and extravascular thermal volume (ETV, 2.6-7.1 ml/g dry intravascular blood-free lung wt, thermal-green dye indicator technique) that were stable by 90 min. Then, bilateral femoral arteriovenous fistulas were opened and closed in 30-min periods to cause reversible increases in QT and associated Qs/QT. When fistulas were open the time-averaged QT increased from 5.1 to 6.9 min (P less than 0.05), the simultaneous Qs/QT rose from 30.7 to 38.4% (P less than 0.05), but ETV did not increase. We conclude that increasing lung edema does not account for our rise in Qs/QT when QT increased.
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PMID:Increased cardiac output increases shunt: role of pulmonary edema and perfusion. 390 79


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