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)

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

Haemodynamic measurements were made on 25 patients with aluminium phosphide poisoning. There was severe hypotension (mean arterial pressure 62.7 +/- 19.3 mmHg) and reduction in cardiac output (2.13 +/- 0.9 lit/min/m2). However, the systemic vascular resistance was only moderately elevated (2050 +/- 732 dynes/m2). The right atrial pressure was increased but the pulmonary artery and pulmonary capillary wedge pressures were normal, even in patients with pulmonary oedema. Thirteen patients (52%) who died had a lower cardiac output (p less than 0.05). Saline infusion significantly improved haemodynamics in some patients. Its judicious use early in the course of treatment may be beneficial.
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PMID:Aluminium phosphide poisoning: haemodynamic observations. 180 Mar 3

Inducing pulmonary edema in rat, air bubbles the diameter of which was about 0.3 mm were continuously infused into the right atrium through a catheter at the rate of 2.8 ml/kg/hr during 0.5, 1 and 2 hours, under controlled ventilation (tidal volume of 9 ml/kg and respiratory rate of 80/min) with 1% halothane in room air. Saline or Dilazep hydrochloride solution was simultaneously infused into the right atrium via another catheter. Pulmonary edema was evaluated by the measurement of the ratio of extravascular water weight of lung (g) to blood-free dry lung weight (g) (EVWW) using the gravimetric method and with histologic studies using the rapid freezing method. In control rats, which were sacrificed immediately after induction of anesthesia, the EVWW was 3.114 +/- 0.121 g/g blood-free dry lung (mean +/- 1 S.D. n = 8). In baseline experiments (2 hours ventilation and saline infusion without air embolization), the EVWW was 3.291 +/- 0.081 (n = 4). In air embolization groups with 2 hours saline infusion, EVWW were 3.756 +/- 0.170 (n = 4), 3.722 +/- 0.170 (n = 4) and 3.731 +/- 0.245 (n = 5) in 0.5, 1 and 2 hours infusion groups, respectively. Regardless of emboli infusion time perivascular cuffs and peribronchial cuffs were revealed in the 2 hour saline infusion groups. In the experiment in which the animals were sacrificed immediately after one hour infusion of air bubbles, there was no evidence of pulmonary edema and the EVWW of 3.060 +/- 0.092 (n = 4) in this group control and baseline were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Induction of pulmonary edema in rat with pulmonary artery air embolization and inhibitory effects of dilazep hydrochloride]. 261 87

Dogs were anesthetized with pentobarbital and placed on a piston ventilator with room air. Ten animals received an endobronchial lavage of normal saline (3 mg/kg). Ten other animals received an endobronchial lavage of the same volume of a nonionic detergent, Tween 20, 5% in saline. Detergent lavage was shown by Wilhelmy balance to increase surface tension of lung extracts. Saline lavage did not alter the surface tension of lung extracts. No significant differences between the groups were noted in cardiac output, left ventricular and diastolic pressure, mean pulmonary artery pressure, or colloid oncotic pressure. Static compliance and arterial PO2 were decreased following detergent lavage. Animals were sacrificed 2 hr after lavage and pulmonary extravascular water volume (PEWV) was measured gravimetrically. Saline-lavaged lungs with normal surface tension had a PEWV of 4.3 ml/g dry lung. Tween-lavaged lungs with increased surface tension had a PEWV of 5.3 ml/g dry lung (P less than 0.005). When the estimated volume of residual lavage solution remaining in the lung parenchyma was subtracted from the total wet lung wt, the corrected PEWV was 3.62 +/- 0.12 ml/g dry lung for saline-lavaged lung and 4.76 +/- 0.19 ml/g dry lung for Tween-lavaged lung. PEWV for 11 control animals ventilated 2 hr without lavage was 3.61 +/- 0.13 ml/g dry lung. It is concluded that, experimentally, high alveolar surface tension can induce pulmonary edema even when pulmonary microvascular hydrostatic and colloid oncotic pressures are normal.
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PMID:High surface tension pulmonary edema. 668 15

The effects of saline infusion (20 ml/kg/30 minutes) and homologous plasma infusion (20 ml/kg/30 minutes) on the lung fluid balance during increased pulmonary capillary permeability secondary to Escherichia coli endotoxin infusion (1 microgram/kg/15 minutes) were studied in unanesthetized sheep. Saline and homologous plasma infusion increased lung lymph flow by 10.6% and 10.8%, respectively. The bloodless wet-to-dry ratio was 5.1 +/- 0.2 in the saline group and 5.2 +/- 0.2 in the homologous plasma group. The saline infusion decreased the plasma oncotic pressure while the plasma infusion increased plasma oncotic pressure. However, the increase in plasma oncotic pressure was negated by concomitant changes in the lymph oncotic pressure and greater increases in pulmonary microvascular pressure during the plasma infusion. Changes in pulmonary microvascular pressure predominated over changes in the oncotic pressure gradient. Both saline and homologous plasma infusion increase fluid filtration into the interstitial space by the same magnitude. Therefore neither has a clear advantage in the treatment of pulmonary edema during increased permeability.
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PMID:Comparison of the effects of saline and homologous plasma infusion on lung fluid balance during endotoxemia in the unanesthetized sheep. 702 Jan 36

Pulmonary surfactant deactivation is an important factor in the pathophysiology caused by wood smoke inhalation. Surfactant replacement is beneficial in treatment of surfactant-deficient neonates and possibly the adult respiratory distress syndrome (ARDS). In this study, the effect of exogenous Exosurf treatment for acute wood smoke injury was examined in four groups of rabbits. All groups were anaesthetized, placed on a ventilator, and surgically prepared for haemodynamic, peak airway pressure (P(aw)), and blood gas measurements. Rabbits were monitored for 2 h following smoke or sham smoke inhalation. At the conclusion of the experiment pulmonary oedema and surfactant function were measured. A Control group (n = 5) was followed without intervention. A Smoke group (n = 4) was ventilated with wood smoke for 3 min. A third group (Smoke+Exo, n = 4) was subjected to smoke followed by pulmonary instillation of Exosurf (5 ml/kg). Saline (5 ml/kg) was instilled into the lungs of the fourth group (n = 3) as a control for Exosurf instillation. Saline, Smoke and Smoke+Exo all significantly lowered PO2 and elevated P(aw) compared to baseline and the Control group. Exosurf treatment did not reduce the pulmonary oedema or restore surfactant function caused by smoke exposure. This study indicates that wood smoke inhalation acutely damages the lung and that administration of Exosurf by instillation is not an effective treatment.
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PMID:Exosurf treatment following wood smoke inhalation. 821 66

Forty-three cases of diabetic ketosis were analysed to determine the mode of presentation, treatment modalities and outcome. Among these cases 62.8% were non-insulin dependent diabetes mellitus (NIDDM) patients and 37.2% belonged to the insulin dependent diabetes mellitus (IDDM) group. Six patients had blood glucose levels of more than 250 mg/dl but less than 300 mg/dl who were grouped separately for analysis under the term "euglycaemic diabetic ketoacidosis (EGDK)". Infection was the commonest precipitating factor in diabetic ketosis in all groups. Abdominal pain and vomiting occurred with NIDDM and EGDK cases. Drowsiness was common and coma was rare. Acute myocardial infarction (MI) and pulmonary oedema occurred with NIDDM cases. Shock, acidosis, acquired respiratory distress syndrome (ARDS) and mucor mycosis were seen with IDDM cases. Mortality was 7 out of 43(16.3%). Saline requirement was lower in NIDDM and EGDK cases. Intensive insulin therapy with hourly intravenous doses were needed for IDDM cases while majority of NIDDM cases could be managed with 6 hourly doses of insulin given subcutaneously or intramuscularly.
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PMID:Changing profile of diabetic ketosis. 956 97

We describe a five-week-old boy who had seizures and extreme hypernatraemia secondary to ingesting an improper home-made formula. Initial sodium concentration was 211 mmol.l-1. Other clinical and biological features were moderate dehydration and renal insufficiency with generous urine output and high urinary sodium concentration. Fluid therapy with hypotonic dextrose solution corrected the volume deficit in 48 h and progressively decreased the serum sodium concentration. During ICU stay the patient developed recurrent episodes of seizures and pulmonary oedema requiring mechanical ventilation for five days. Recovery was complete with no abnormal sequelae after a ten-month follow-up. Salt poisoning is in unusual cause of extreme hypernatraemia. It can be safely managed with fluid therapy alone if urine output is preserved, with progressive decrease of serum sodium as target. If this condition is recognized, outcome should be favourable.
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PMID:The management of extreme hypernatraemia secondary to salt poisoning in an infant. 1071 47

Doxorubicin is a chemotherapeutic agent that can induce cardiotoxicity and congestive heart failure (CHF). In this study we tested whether intracoronary Akt1 gene delivery could inhibit doxorubicin-induced CHF. Saline or a replication defective adenoviral vector expressing constitutively-active Akt1 (myrAkt) or beta-galactosidase (betagal) was delivered to the myocardium of 8 week old rats one day prior to initiating doxorubicin administration. In animals receiving saline or betagal, doxorubicin resulted in significant decreases in cardiac function and retarded post-natal heart growth at the 5 weeks time point. In contrast, transduction of myrAkt protected hearts against doxorubicin-induced decreases in fractional shortening and cardiac index, and improved left ventricular function at 5 weeks time point. Delivery of myrAkt also reversed the doxorubicin-induced reduction in post-natal heart growth and diminished lung edema. These data show that myocardial Akt can inhibit doxorubicin-induced reductions in cardiac function and growth, suggesting that manipulation of this signaling pathway may have utility for the treatment of congestive heart failure.
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PMID:Elevated myocardial Akt signaling ameliorates doxorubicin-induced congestive heart failure and promotes heart growth. 1239 81

Fluid and electrolyte balance is often poorly understood and inappropriate prescribing can cause increased post-operative morbidity and mortality. The efficiency of the physiological response to a salt or water deficit, developed through evolution, contrasts with the relatively inefficient mechanism for dealing with salt excess. Saline has a Na+:Cl- of 1:1 and can produce hyperchloraemic acidosis, renal vasoconstriction and reduced glomerular filtration rate. In contrast, the more physiological Hartmann's solution with a Na+:Cl- of 1.18:1 does not cause hyperchloraemia and Na excretion following infusion is more rapid. Salt and water overload causes not only peripheral and pulmonary oedema, but may also produce splanchnic oedema, resulting in ileus or acute intestinal failure. This overload may sometimes be an inevitable consequence of resuscitation, yet it may take 3 weeks to excrete this excess. It is important to avoid unnecessary additional overload by not prescribing excessive maintenance fluids after the need for resuscitation has passed. Most patients require 2-2.5 litres water and 60-100 mmol Na/d for maintenance in order to prevent a positive fluid balance. This requirement must not be confused with those for resuscitation of the hypovolaemic patient in whom the main aim of fluid therapy is repletion of the intravascular volume. Fluid and electrolyte balance is a vital component of the metabolic care of surgical and critically-ill patients, with important consequences for gastrointestinal function and hence nutrition. It is also of importance when prescribing artificial nutrition and should be given the same careful consideration as other nutritional and pharmacological needs.
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PMID:Fluid, electrolytes and nutrition: physiological and clinical aspects. 1537 58


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