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

The most important component of the renal-body fluid feedback is renal pressure natriuresis which through sodium and water excretion stabilizes arterial pressure. The chronic effects of angiotensin II in regulating the pressure natriuresis was studied in dogs by the Guyton school. Renal perfusion was either permitted to increase or was maintained constant with a servo-controlled occluder placed on the abdominal aorta just above the kidneys. When the renal pressure was allowed to increase, sodium excretion was reduced for a day and after 4-5 days there was little net change in sodium balance and arterial pressure stabilized at about 30 mm Hg above control. In the servo-controlled renal perfusion, escape from sodium retention did not occur, arterial pressure continued to rise, and pulmonary edema developed. Angiotensin II, by its hemodynamic and tubular effects, modulates renal sodium and water excretion and has an important role in blood pressure regulation. Antibodies to renin and converting enzyme inhibitors showed a causal relationship between the stimulated renin-angiotensin system and the antihypertensive effect of these agents. Chronic effects are observed in hypertensive patients with normal or even low plasma renin activity. This suggests that local angiotensin concentrations in the vascular and renin tissues may be more important in determining sodium and water excretion. Our knowledge of the renin-angiotensin system in regulating blood pressure made the usage of converting enzyme inhibitors a logical and efficacious modality in the therapy of hypertension. In a multicenter study of 202 hypertensive patients, the efficacy and safety of ramipril and enalapril was studied.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The renin-angiotensin system, the kidney, and hypertension. 247 96

Evidence has been accumulating that regulation of the rate of solute and fluid removal from the alveolar spaces may play an important role in the prevention and/or resolution of alveolar pulmonary edema. In this study, the isolated perfused rat lung was used to investigate the effects of an adenosine 3',5'-cyclic monophosphate (cAMP) analogue or a phosphodiesterase inhibitor on active sodium transport from airspace to vascular space. Three tracers were instilled into the airways of isolated Krebs-Ringer bicarbonate solution (KRB)-perfused rat lungs. The appearance of tracers in the single-pass perfusate was measured, and the apparent permeability-surface area products (PS) were calculated for each tracer at each sample time based on Fick's first law of diffusion. After steady-state PS values had been reached, a cAMP analogue or phosphodiesterase inhibitor was added to the perfusate. Both agents caused significant increases in the PS for 22Na. In another group of experiments, a cAMP analogue was added to the perfusate, followed by the subsequent addition of a sodium transport inhibitor and the resultant large decrease in the PS for 22Na. These data are consistent with the regulation of active sodium transport across the intact mammalian alveolar epithelium by a cAMP-mediated process leading to removal of sodium from the alveolar spaces, with anions and water following passively.
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PMID:Evidence for regulation of sodium transport from airspace to vascular space by cAMP. 247 37

The effect of the detergent dioctyl sodium sulfosuccinate on pulmonary extravascular water volume (PEWV) was studied in adult anesthetized mongrel dogs. The detergent was dissolved as a 1% solution in a vehicle of equal volumes of 95% ethanol and normal saline and administered by ultrasonic nebulizer attached to the inspiratory tubing of a piston ventilator. Two hours following detergent aerosol PEWV measured gravimetrically was increased compared with either animals receiving no aerosol or those receiving an aerosol of vehicle alone. Loss of surfactant activity and increased alveolar surface tension were demonstrated by Wilhelmy balance studies of minced lung extracts, by a fall in static compliance, and by evidence of atelectasis and instability noted by gross observation and by in vivo microscopy. No significant changes in colloid oncotic pressure or pulmonary microvascular hydrostatic pressure were observed. These data suggest that pulmonary edema can be induced by increased alveolar surface tension and support the concept that one of the major roles of pulmonary surfactant is to prevent pulmonary edema.
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PMID:High surface tension pulmonary edema induced by detergent aerosol. 257 44

The effects of PEEP and subsequent augmentation of cardiac output by sodium nitroprusside (SNP) were examined in a canine model of asymmetric oleic acid injury to the right lung. PEEP (9.2 +/- 0.5 cm H2O) was added to six animals to decrease venous admixture (Qsp/Qt) from 50.6 +/- 4.4% to 16.0 +/- 1.3% (p less than .05). With PEEP, intrapulmonary blood flow distribution (assessed by radioactive microspheres) decreased significantly to nondependent lung regions while increasing to dependent regions. In six other animals, zero end-expiratory pressure (ZEEP) did not alter intrapulmonary blood flow distribution. SNP was then administered to increase cardiac output by 40% (to 2.60 +/- 0.21 L/min in the ZEEP group and to 1.75 +/- 0.27 L/min in the PEEP group). SNP produced no adverse effects on Qsp/Qt or intrapulmonary blood flow distribution. Specifically, SNP did not preferentially dilate pulmonary vessels injured by oleic acid with or without end-expiratory pressure. Thus, administration of a vasodilator drug in asymmetric pulmonary edema appears well tolerated.
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PMID:Sodium nitroprusside and positive end-expiratory pressure are not detrimental in canine asymmetric pulmonary edema. 264 70

Hypernatremia is a potentially life-threatening electrolyte abnormality. This problem develops most often because of loss of water from the animal, but in rare cases hypernatremia results from gain of sodium chloride. Important conditions predisposing to hypernatremia include diarrhea, vomiting, heat stroke, fever, limited access to water, excessive diuretic use, renal diseases, and pituitary diabetes insipidus. This condition rarely develops if animals have adequate access to water. Clinical signs relate to central nervous system derangements and can progress to seizures and coma. Diagnosis is based on the serum sodium concentration; treatment should be instituted if it is greater than 170 mEq per L. Treatment is based on knowledge of the volume status of the patient and the probable cause for the hypernatremia. In general, 5 per cent dextrose in water or other hypotonic fluids are given slowly intravenously. The rate of administration should be adjusted so the water deficit is replaced over 48 to 72 h. Too rapid correction of hypernatremia can lead to cerebral edema and worsening of the animal. In cases of salt intoxication, diuretics must be given in addition to slow water replacement to avoid the development of pulmonary edema.
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PMID:Hypernatremia. 264 64

Exercise and physical fitness are becoming increasingly popular in our society. As a result there are more individuals who are at risk for the development of acute respiratory emergencies associated with sports and athletics. EIB is a common feature of asthma and is characterized by a postexercise fall in FEV1 of more than 10 per cent. Although a variety of medications have been used for the prevention of EIB, cromolyn sodium and inhaled adrenergic agonists have been shown to be the most effective. EIA and cholinergic urticaria are two physical allergies in which hypotension can be brought on by exercise. In some individuals, EIA develops only in association with the ingestion of a particular food. Associated with sports and recreational activities in alpine areas is the risk of developing acute high-altitude medical problems. One of the most dramatic and potentially life threatening is high-altitude pulmonary edema. The management of this condition can be problematic, particularly if rapid descent to lower elevations is not possible. Although rare, spontaneous pneumothorax and pulmonary emboli do develop in the otherwise well-conditioned athlete. These entities must be considered when the physician evaluates any athlete in whom acute cough and dyspnea develop.
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PMID:Acute respiratory emergencies in emergency treatment of the injured athlete. 266 79

We studied the formation of pulmonary edema on 9 patients with paraquat poisoning using thermal-sodium double indicator dilution method for the measurement of lung water. In survivors group (n = 4) extravascular thermal volume (EVTV) was not almost changes. In non-survivors group (n = 5) EVTV increased about three times as much as that in survivors group on 32 hours after admission. EVTV was correlated with PCP-PCOP in both survivors group and non-survivors group (n = 64, r = 0.665, p less than 0.01). But EVTV in non-survivors group was higher than that in survivors group within same PCP-PCOP. In non-survivors group delta EVTV/delta (PCP-PCOP) in 24 hours after admission was correlated with initial PCP-PCOP (r = 0.984, p less than 0.01). We propose that the formation of pulmonary edema on paraquat poisoning is mainly due to the increased capillary permeability, influenced by the increased pressure gradient of capillary barrier.
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PMID:[A clinical study of pulmonary edema on paraquat poisoning by double indicator dilution method using heat and sodium]. 266 31

Several cases of hyponatremia, with symptoms including altered mentation, seizures, and pulmonary edema, have been reported in endurance athletes over the last few years. This condition has been observed most frequently in individuals participating in ultra-distance events but has also been reported in a marathon runner. Excessive water intake has been identified as a common etiological factor. Given that this is a serious condition but that the risks of impaired performance and heat injury from inadequate water ingestion are substantial, how likely is it that hyponatremia will develop in events of marathon duration or shorter? A review of fluid and electrolyte balance--and an example of expected sodium and fluid losses in a marathon runner--suggest that normal regulatory mechanisms should prevent its occurrence in the absence of other contributing factors. Accordingly, ingestion of adequate fluid should remain a priority for individuals engaged in endurance activity.
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PMID:Water: can the endurance athlete get too much of a good thing? 268 35

Adult respiratory distress syndrome (ARDS) is a non-cardiogenic pulmonary edema of various etiologies. Here we report the first application of proton nuclear magnetic resonance (NMR) for the detection of abnormal metabolites in plasma from patients with ARDS. By comparing plasma obtained from the systemic artery with that obtained from the pulmonary artery, we could study the metabolic status of the lung in patients with ARDS. Although their concentrations may vary, the peaks for acetate, acetoacetate, beta-hydroxybutyrate, phenylalanine, and other unidentified compounds in water-suppressed NMR of these patients' plasma were higher than in the normal controls. The proton NMR resonance at a chemical shift of about 7.4 ppm (relative to sodium tetradeutero-3-trimethyl-silylpropionate), presumably caused by phenylalanine and its related metabolites produced by a disordered amino acid metabolism, is detected in greater than 65% of the samples from ARDS patients. We discuss the detection of abnormal metabolites in terms of possible deranged metabolism of carbohydrates, lipids, or amino acids in this syndrome.
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PMID:Proton nuclear magnetic resonance studies of plasma to determine metabolic status of patients with adult respiratory distress syndrome. 270 52

This study was designed to test whether intraperitoneally injected sodium hydrosulfide (NaHS) would mimic the pulmonary alterations induced by lethal peracute exposure to an atmosphere containing hydrogen sulfide. Groups of five Sprague-Dawley rats were exposed to an atmosphere of either 2317.6 +/- 547.3 mg m-3 H2S (H2S group) or no H2S (air group), or were injected intraperitoneally with a solution containing 30 mg kg-1 sodium hydrosulfide (NaHS group) or saline solution (vehicle control). Rats of the air and saline groups were killed by cervical dislocation. All rats exposed to H2S or injected with NaHS died within 3 min; however, only rats exposed to H2S showed severe respiratory distress in the agonic phase preceding death. In addition, rats in the H2S group had a notable discharge of serous fluid from the mouth and nostrils. At necropsy, all rats in the H2S group had gross and histologic evidence of pulmonary edema characterized by massive extravasation of eosinophilic fluid into the bronchoalveolar space. In contrast, the lungs of rats injected with NaHS or saline or exposed to air were unaffected. It was concluded that the edematogenic effect of H2S in the lungs cannot be reproduced by injection of NaHS. The severity of lung edema induced by a peracute exposure to H2S was extensive enough to account for death.
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PMID:Peracute toxic effects of inhaled hydrogen sulfide and injected sodium hydrosulfide on the lungs of rats. 271 35


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