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

We compared the effects of continuous positive-pressure ventilation (CPPV), using 10 cmH2O positive end-expiratory pressure (PEEP), with intermittent positive-pressure ventilation (IPPV), on pulmonary extravascular water volume (PEWV) and lung function in dogs with pulmonary edema caused by elevated left atrial pressure and decreased colloid osmotic pressure. The PEWV was measured by gravimetric and double-isotope indicator dilution methods. Animals with high (22-33 mmHg), moderately elevated (12-20 mmHg), and normal (3-11 mmHg) left atrial pressures (Pla) were studied. The PEWV by both methods was significantly increased in the high and moderate Pla groups, the former greater than the latter (P less than 0.05). There was no difference in the PEWV between animals receiving CPPV and those receiving IPPV in both the high and moderately elevated Pla groups. However, in animals with high Pla, the Pao2 was significantly better maintained and the inflation pressure required to deliver a tidal volume of 12 ml/kg was significantly less with the use of CPPV than with IPPV. We conclude that in pulmonary edema associated with high Pla, PEEP does not reduce PEWV but does improve pulmonary function.
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PMID:Effects of continuous positive-pressure ventilation in experimental pulmonary edema. 0 21

The pathogenesis of shock lung as well as the success of therapy in this condition was studied in 79 cases of extrathoracic trauma. The water-, hemoglobin-, and DNA contents of the lungs were measured in order to determine the extent of edema, the rate of perfusion, and proliferation. The cases were divided into two groups according to whether they had or had not received medical therapy before death. The data from these two groups were compared using statistical methods in which time of survival was especially taken into account. The fluid balance, pO2, pCO2, central venous pressure, pH of the serum, total serum protein and serum creatinine were also studied in these cases. Results of the study are as follows. Three phases of the posttraumatic syndrome of shock-lung could be distinguished: phase I (initial phase): blood perfusion is increased, edema is beginning to form, and medical treatment has not yet begun. Phase II (early phase = sydrome of early respiratory failure): pulmonary edema is developing rapidly while perfusion is decreasing. Phase III (late phase = syndrome of late respiratory failure): proliferative changes predominante and the edema is still increasing. The mean weight of the lungs was 397 g (s = 170) in phase I, 774 G (S = 361) In phase II, and 1124 g (s = 310) in phase III. The survival times correlated significantly and positively with the amount of water and DNS in the lungs and significantly and negatively to the amount of hemoglobin in the lungs. Thus, increasing pulmonary edema and increasing proliferative changes occurred with decreasing pulmonary perfusion. This correlation was even noted in groups of patients who had not received medical treatment and whose survival times were short. In treated cases, the fluid balance was significantly and negatively correlated to the total serum protein.
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PMID:[Examinations to phenomenon of shock-lung (author's transl)]. 0 60

Patients who are victims of near drowning in fresh water or salt water very frequently have acute edema of the lung which occurs either immediately, or after a free interval of variable duration. The mechanism of this edema is explained, in near drowning in salt water, by the hyperosmolarity of the alveolar fluid leading to a seeping of plasma from the capillaries in the alveoli. In the case of near drowning in fresh water, it is on the contrary the inhaled liquid which passes into the circulation, therby leading to immediate hypervolemia, but this overload is only transitory and is not responsible for the pulmonary edema which occurs later is not accompanied by a rise in pulmonary capillary pressure. It is therefore a lesional edema as is certified by the anatomopathological modifications found in the lungs of drowned patients. Therapeutic management must therefore take into consideration this physiopathology of acute edema of the lung in the drowned.
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PMID:[Pulmonary edemas of drownings]. 0 52

Whatever the etiology of pulmonary edema, i.e. increase in intrapulmonary water, edema passes through three, moreover intricate phases: 1- intracellular edema clearly visible in the type 1 pneumocyte. This intracellular edema appears at the same time as: 2- interstitial edema; that which appears when: 3- numerous vesicules of pinocytosis and separation of the capillary endothelial cells account for it; 4- intra-alveolar edema itself appears later and corresponds to the major clinical phase of pulmonary edema. There is nothing surprising about this as the cellular functions of pneumocytes are impervious as can be shown for example by studies carried out with tracers. This intracellular alveolar edema seems to have two different aspects depending on whether the experimental conditions create an acute or sub-acute pathology. In the acute form, the edema is poor in lipids and in proteins. In the sub-acute of chronic forms, it is on the contrary very rich in them. 5-In the last phase, a veritable desquamation of the pneumocytes then of the endothelial cells is produced which is very frequently lethal. If survival occurs, two sorts of lesions are found: -colonisation of the alveolar surface with type II pneumocytes; - occurrence of possible intersitial fibrosis. The remarkable fact is that such lesions are visible in a more or less identical manner in all cases of pulmonary edema, whether they be hemodynamic or lesional. The morphology does not confirm this physiopathological distinction which is moreover questionable as all pulmonary edema become lesional sooner or later.
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PMID:[Pulmonary edemas. Anatomic study]. 0 62

All hypervolemia or any decrease in plasma oncotic pressure leads to deterioration in lesional pulmonary edema. The aim of albumin infusions is to restore the plasma oncotic pressure and to oppose the passage of water into the extravascular space. This therapy is however debatable owing to the abnormal increase in the permeability of the alveolo-capillary membrane to proteins. Diuretics enable one to lower the volemia and to maintain the pulmonary capillary pressure at its minimum level. However, strict hemodynamic supervision is absolutely necessary. Cortico-steroids have been recommended without serious physiopathological justification. However, they have a preventive action on interstitial edema in endotoxic shock.
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PMID:[Reduction and anti-inflammatory technics in non-hemodynamic pulmonary edemas]. 0 65

Several clinical reports of salicylate-induced pulmonary edema led us to investigate the mechanism in a chronic unanesthetized sheep preparation. We infused an aspirin-buffer solution intravenously at rates up to 1,200 mg of aspirin per hour and compared effects on lung lymph flow and lymph protein concentration to those seen after mechanical elevation of pulmonary vascular pressures. Aspirin had little effect on lung vascular pressures but caused lung lymph flow to increase an average of greater than twice baseline. Because lymph protein concentrations were higher for a given lymph flow with aspirin than during mechanical pressure elevation, lymph protein (lymph flow X lymph to plasma protein concentration) increased much more with aspirin. Thus, aspirin appears to cause increased permeability to fluid and protein in the pulmonary vascular bed. Aspirin caused arterial PO2 to decrease from 83 +/- 3 SE mm Hg to 74 +/- 3 mm Hg (P less than 0.05) and caused postmortem extravascular lung water to increase. These findings are supported by a review of the clinical literature, indicating that salicylate pulmonary edema in humans is noncardiac in origin and may occur at doses considered therapeutic for some diseases as well as after overdose.
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PMID:Salicylate pulmonary edema: the mechanism in sheep and review of the clinical literature. 1 76

Cardiopulmonary resuscitation and rewarming were successful in a 5-year-old boy who had been submerged for 40 minutes in ice-cold fresh water. Severe metabolic acidosis was corrected by intravenous infusion of sodium bicarbonate solution before spontaneous circulation could be re-established. Fulminant pulmonary oedema developed after re-establishment of spontaneous circulation. This was efficiently reversed by positive-end-expiratory-pressure ventilation. During 2 days of treatment of a respiratory the patient gradually regained consciousness; the endotracheal tube was then removed and the patient immediately started talking intelligently. The patient went through a period of slow cerebration and motor dysfunction but recovered rapidly, and on examination 13 months after the accident all findings were normal.
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PMID:Survival after 40 minutes; submersion without cerebral sequeae. 4

The study concerns the action of dehumidified or humidified gas on the pulmonary lining layer. The results of our research suggest that water vapor used in artificial ventilation may be an important determining factor of the respiratory problems reported by clinicians in man. Important modifications of the lining layer of the alveolar epithelium occur, accompanied by more important alterations, including those of the content of the alveolus, all of which contribute to the pulmonary edema observed.
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PMID:The action of humidified gas on the pulmonary lining layer. Ultrastructural observations after administration of pure oxygen and of various mixtures of oxygen and carbon dioxide. 12 59

Rats were exposed under static conditions to phosgene at concentrations within the LCt50 range and above. Lungs were removed at various postexposure intervals. Degrees of pulmonary edema were estimated by increases in percentage of water in the lungs of exposed groups as opposed to control animals. Lungs were fractionated into four major subcellular organelle fractions: nuclear debris, mitochondrial-lysosomal, microsomal, and soluble (cytoplasmic). Activities of p-nitrophenyl phosphatase, cytochrome C oxidase, ATP'ase, and LDH within these fractions were decreased after phosgene exposure. There was a concomitant increase in serum LDH levels. One possible mechanism that may play a role in phosgene damage can be associated with either inhibition or loss of enzyme activities from the lung.
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PMID:Effect of phosgene on rat lungs after single high-level exposure. 20 Dec 20

The purpose of this study was to examine the in vivo effects of acute exposure to a cadmium chloride aerosol on the activity of pulmonary enzymes and selected physiologic parameters that are altered by exposure to oxidant agents. Male rats were exposed for 1 hour to 0.5 per cent aerosol of cadmium chloride. At 1,5, and 11 days after exposure to cadmium chloride, exposed rats compared to control rats (data expressed as per cent of control values) had lung-to-body weight ratios of 192, 174, and 140 per cent; lung glucose-6-phosphate dehydrogenase activities of 90, 107, and 135 per cent; lung superoxide dismutase activities of 96, 101, and 132 per cent; tidal volumes of 62, 63, and 89 per cent; respiratory frequencies of 170, 145, and 108 per cent; and lung weight-specific static deflation volumes at 30 cm water of 30, 13, and 31 per cent. A zero-order clearance of cadmium from whole lung was observed, with a half-time of 27.4 days. Light microscopic examination of lung tissue revealed initial pulmonary edema on day 1 that progressed to interstitial pneumonitis on day 5, with some recovery by 11 days after exposure. The cadmium induced biochemical, physiologic, and pathologic alterations were similar to the responses observed in lungs of rats exposed to a wide variety of pulmonary irritants; thus, the changes observed may represent a nonspecific response to tissue injury.
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PMID:Biochemical and physiologic changes in lungs of rats exposed to a cadmium chloride aerosol. 21 68


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