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

A method for measuring pulmonary oedema (ETVL) is described using sodium ions as the intravascular indicator and heat as the extravascular indicator. The technique offers the advantage of virtually unlimited repeatability, relatively uncomplicated instrumentation and no blood loss. There is also the potential for differentiating between pulmonary oedema and pulmonary congestion and determining the efficacy of therapy. A sensing catheter to detect blood conductivity and temperature changes is required. Ideally the sensing catheter should be situated at a point just distal to the aortic valve. However, a commercially manufactured detecting catheter we had built proved troublesome to insert because of its relatively large diameter. Therefore, an external sensing catheter has been constructed to measure ETVL and the values obtained have been compared with those from an internal catheter. There was no difference between the internal and external catheter QT, but ETVL was consistently overestimated by 2.46 +/- 0.26 ml/kg. However, this value can be related to the internal value and can be used for clinical studies.
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PMID:Lung water estimation using an external sensing catheter. 87 37

Evidence from isolated bovine pulmonary vessels and respiratory smooth muscles suggests that bovine slow-reacting substance of anaphylaxis (SRS-Abov) may contribute to bronchoconstriction and pulmonary oedema during anaphylaxis in cattle. Bovine bronchus is sensitive to low concentrations of SRS-Abov and is considerably more sensitive than trachea. Contraction of the calf bronchus to SRS-Abov can be antagonized by sodium meclofenamate, suggesting prostaglandins may be involved in the contraction. Bovine pulmonary artery did not contract to SRS-A at any of the concentrations examined. None of the proposed SRS-A receptor antagonists, FPL 55712, PR-D-92-EA, or sodium meclofenamate, inhibit the effects of bovine SRS-A in bovine pulmonary vein.
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PMID:Effects of bovine SRS-A (SRS-Abov) on bovine respiratory tract and lung vasculature in vitro. 88 66

Five patients with severe acidosis and pulmonary oedema complicating cholera were seen at the Cholera Research Laboratory, Dacca, in a two-year period. All had had inadequate treatment. Their disease resulted in acidosis prior to admission; only the two who subsequently survived received volumes of sodium bicarbonate solutions sufficiently large to repair completely their acidosis. Saline alone worsened pulmonary congestion, while alkali appeared to relieve it despite the accompanying volume expansion. These observations are consistent with the known redistribution of blood to the central circulation in acidosis. Timely and proper treatment of cholera will avert this syndrome, when use of isotonic sodium bicarbonate sufficient to correct acidosis may be very helpful.
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PMID:Pulmonary oedema associated with acidosis in patients with cholera. 97 48

Changes in intracellular water content appear to be common abnormalities induced by a wide variety of pathogenic mechanisms. Such changes in cell water produce changes in the water in various subcellular organelles bound by semipermeable membranes. Cell and subcell functions then alter in their turn. In isolated alveolar macrophages (rabbit), intracellular and intramitochondrial oedema reduces mitochondrial O2 utilization. Metabolic control is maintained because lactate production reverses (Pasteur effect). On reconstitution, O2 utilization and lactate production return towards normal, indicating reversibility. Cellular and intramitochondrial dehydration also reduces mitochondrial O2 utilization but metabolic control is lost because lactate production also decreases. Osmotic reconstitution does not reverse the abnormality. Exposure to hypotonic media leads to release of lysosomal enzymes (beta-glucuronidase, EC 3.2.1.31) to the extracellular phase of isolated alveolar macrophages. Some of this release is caused by exocytosis although, at low osmotic concentrations, intralysosomal oedema ultimately ruptures lysosomes, with extensive discharge of enzyme. In turn, lysosomal enzymes may injure more normal cells. Impairment of energy metabolism caused by hypoxia leads to intracellular oedema, because Na+ accumulates in the cells when ATP is no longer available for the sodium pump. Continued studies of the disorders in cell physiology caused by changes in cell and subcell water should provide important new insights into a wide variety of disease states (including pulmonary oedema).
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PMID:Intracellular and subcellular oedema and dehydration. 104 40

The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.
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PMID:[Physiopathology of accidental drowning]. 112 62

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.
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PMID:Fatal self-administration of sodium azide. 114 58

Ten normal healthy male subjects between 20-30 years of age were initially examined at Delhi (200 m) and thereafter air-lifted to an altitude of 3,500 m. Excretion of sodium, potassium and chloride in urine and their plasma level were determined at sea level (SL) and daily at high altitude (HA) for 4 d. At HA, four subjects developed high-altitude pulmonary edema (HAPE), four remained normal, and two suffered from acute mountain sickness. The results on normals and HAPE are presented. There was increased excretion of potassium at HA in both groups resulting in reduction of plasma level. The sodium and chloride excretion was also increased in normals at HA irrespective of urine volume. In HAPE cases, the sodium and chloride excretion was related to urine output. With the retention of fluid, the excretion of these ions in urine was diminished without a parallel change in plasma levels.
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PMID:Electrolyte changes at 3500 m in males with and without high-altitude pulmonary edema. 114 75

Pulmonary edema and plasma kininogen consumption caused by intravenously administered adrenaline, were inhibited in rats pretreated with acetylsalicylic acid, but not in rats pretreated with indomethacin or sodium salicylate. The possibility of a connection between this edema and mast cell-linked activation of kallikrein by adrenaline is discussed, as well as the possible role of acetylsalicylic acid acting as an acetylating inhibitor of these processes.
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PMID:Acute pulmonary edema and plasma kininogen consumption in the adrenaline-treated rat: inhibition by acetylsalicylic acid and resistance to salicylate and indomethacin. 116 Oct 51

A clinical and investigative study is reported of 19 patients with 'idiopathic oedema of women'. The resons for defining this as a specific syndrome unrelated to the menstrual cycle are given, and the clinical features reviewed. During a forced water diuresis the flow and composition of the urine and the plasma volume were studied on tilting from the supine to the upright position seven premenopausal and four postmenopausal patients with this disorder. No differences were found in the results obtained in the follicular and luteal phases of the menstrual cycle or in the pre- and post-menopausal patients. The reductions in urinary volume and electrolyte excretion on upright tilting were greater than those observed under similar circumstances during the luteal phase of the menstrual cycle in normal female controls, and attributed to increased proximal renal tubular reabsorption. The rate of loss of isotopically labelled albumin from the intravascular compartment was greater in patients with idiopathic oedema than in control subjects. A reduction in blood volume on tilting occurred in control subjects and patients with idiopathic oedema, but was greater in the latter; and the larger the fall, the greater were the reductions in urinary flow and electrolyte excretion. The effect of administering 9-alpha-fluorohydrocortisone was studied in nine patients with idiopathic oedema. One patient failed to 'escape' from the sodium-retaining action of this mineralocorticoid and developed pulmonary oedema; the others 'escaped' normally. The pathophysiological disturbance in this condition is related to increased loss of fluid from the vascular compartment but the precise aetiological mechanism remains unknown.
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PMID:Idiopathic oedema of women. A clinical and investigative study. 125 99

Patients with shock lung syndrome were identified as those who developed acute respiratory failure after a profound episode of hypotension secondary to hemorrhagic, gram-negative, or endotoxic shock. In this study, each of the 10 patients with shock lung syndrome received methylprednisolone sodium succinate, 30 mg. per kilogram, intravenously every 6 hours for 48 hours. In addition, all patients were supported with mechanical ventilation, with or without positive end-expiratory pressure (PEEP). Arterial oxygenation improved markedly, and pulmonary edema resolved in all patients. Nine were discharged from the hospital and one died subsequently of disseminated intravascular coagulation. This study demonstrated a significant improvement in mortality rate with repeated pharmacologic doses of methylprednisolone compared to previously reported mortality rates of 60 to 90 per cent in patients with shock lung syndrome treated without repeated pharmacologic doses of steroid therapy.
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PMID:Methylprednisolone. Pharmacologic doses in shock lung syndrome. 126 66


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