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

Lung prostaglandins (PGs) play a key role in normal pulmonary vascular regulation. We investigated PG metabolism during edema formation following paraquat-induced damage with an isolated perfused rat lung preparation. Lungs perfused with paraquat (PQ), 1 X 10(-7) M to 1 X 10(-2) M, showed significant increases in PGF2 alpha prior to detectable functional and pathological changes (increases in airway resistance, vascular resistance, and edema). No changes in PGE were observed. PGF2 alpha in perfused lungs showed a dose-related response following PQ exposure (up to 300% increase over control values). Lungs perfused with PQ and ventilated with high oxygen (95% O2-5% CO2) instead of air-5% CO2 showed a dramatic potentiation in the selective increase of PGF2 alpha, with levels reaching over 1 ng/ml (a 2600% increase over control values). The addition of exogenous PGF2 alpha to the perfusate without PQ initiated edema in a dose-related fashion, indicating the potential of PGF2 alpha as a causative agent in lung edema formation from PQ injury. The addition of ibuprofen (a nonsteroidal anti-inflammatory agent) to the perfusion medium blocked endogenous release of PGF2 alpha in lungs linked to oxidant-induced edema. These data show that in the perfused lung: (1) PQ caused a selective increase of PGF2 alpha; (2) this selective increase occurred prior to the onset of edema; (3) exogenous PGF2 alpha alone induced pulmonary edema; and (4) ibuprofen, in doses which blocked PGF2 alpha, also prevented edema formation.
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PMID:Selective action of prostaglandin F2 alpha during paraquat-induced pulmonary edema in the perfused lung. 657 98

285 patients affected by carbon monoxide poisoning were admitted in our intensive care unit over a period of two years (from july 1980 to july 1982). 18 patients had a pulmonary edema (P.E.). The occurrence of P.E. was more frequent when coma was grade 2, 3 or 4 (p less than 10(-3]. The acute physiologic score (weighting of physiologic measurements) as proposed by Knauss is higher in patients with P.E. (p less than 10(-2]. However death is never due to P.E.; about 54 patients with coma, 5 died; death is related to neurologic aggravation. Neurologic sequelae are not related to the occurrence of P.E. but to a delay in hyperbaric oxygen therapy. These date show that prognosis of carbon monoxide poisoning is related to neurological status and is not influenced by the occurrence of P.E. when correctly treated and when hyperbaric oxygen therapy is early realized.
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PMID:[Acute pulmonary edema in carbon monoxide poisoning. Prognostic effect]. 666 88

The authors report 7 cases of acute pulmonary edema in acute carbon monoxide poisoning. Hemodynamic data suggest existence of a myocardial failure as a possible cause of these pulmonary edema and indicate caution for volemic expansion during the treatment of shock in carbon monoxide poisoning.
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PMID:[Acute carbon monoxide poisoning: lung injury or cardiogenic pulmonary edema?]. 666 89

Air pollution may affect athletic performance. In Los Angeles, contaminants include carbon monoxide, ozone, peroxyacetylnitrate (PAN) and nitrogen oxides, whereas in older European cities, such as Sarajevo, "reducing smog" of sulfur dioxide is the main hazard. The carbon monoxide and ozone levels expected in Los Angeles this summer could affect the athletes' performance in endurance events at the Olympic Games. Carbon monoxide may also impair psychomotor abilities, and PAN causes visual disturbances. The only likely physiologic consequence from reducing smog is an increase in the workload of the respiratory system and thus a decrease in endurance performance. While carbon monoxide has been blamed for myocardial infarctions, nitrogen oxides for pulmonary edema and sulfur dioxide for deaths due to respiratory failure, the only illnesses that are likely to be more frequent than usual among young athletes exposed to high levels of these pollutants are upper respiratory tract infections. Therapeutic tactics include the avoidance of pollution, the administration of oxygen, vitamin C and vitamin E, and general reassurance.
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PMID:Athletic performance and urban air pollution. 674 56

A cardiorespiratory monitoring system allows the measurement of FAECO2 and FECO2 in the expired air of the patient at the mouth (endtidal CO2) and in a mixing box. From these parameters, combined with the measured PACO2, the alveolo-expired (DuA = PECO2/PAECO2) and alveolar-arterial (Dua = PAECO2/PACO2) ductances which assimilate the respiratory system to a two-stage exchanger have brought about a lot of valuable information 1. DuA improves by 20% in 20 patients after removal of bronchial obstruction (p < 0.001) and by 9% in 7 intubated patients after tracheotomy (p < 0.02). DuA falls by 15% (p < 0.001) in 10 patients with hypocapnia (PaCO2 = 28 mmHg) after a dead space adjunction with the aim of normalizing PaCO2 (paCO2 = 35 mmHg). 2. Dua falls by 33% in six patients after pulmonary embolism, proved by angiography (p 0.001) by 9% in 34 patients after 30 min of pure oxygen breathing (p 0.001). On the other hand, inthe absence of clinical or radiological pulmonary edema, in increases by 19% in 38 patients with hypervolemia after diuresis (furosemide) (p < 0.001). Thus since DuACO2 varies with anatomical dead space and the air distribution disorder, DuaCO2 evolves according to the disorders of the blood distribution and arterial-alveolar diffusion. The determination of these coefficients, in the absence of significant changes in the arterial blood gases, helps the diagnosis, guides the early treatment and allows for the monitoring of its efficiency.
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PMID:The continuous monitoring of CO2 ductances in pulmonary intensive care. 677 20

Noncardiogenic pulmonary edema occurred in an anesthetized patient during an otherwise uneventful laparotomy. Following transfusion of an individual unit of whole blood, routine intraoperative monitoring detected sudden major pulmonary shunting (increased alveolar-arterial oxygen gradient) and an increased physiological alveolar dead space (increased arterial-alveolar carbon dioxide gradient). The noncardiac pulmonary edema probably resulted from the presence of a leukoagglutinin against the patient's granulocytes in the donor's plasma. This antibody had no apparent specificity for known HLA, neutrophil, or blood group antigens. The acute respiratory failure was transient, resolving in 72 hours with respiratory support. The presence of otherwise unexplained noncardiogenic pulmonary edema during or soon after a blood transfusion should suggest the possible diagnosis of a leukoagglutinin reaction.
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PMID:Pulmonary shunting during leukoagglutinin-induced noncardiac pulmonary edema. 677 4

A carbon monoxide (CO)-intoxicated patient developed increased permeability-type pulmonary edema demonstrated by a normal capillary wedge pressure and production of protein-rich edema fluid. To investigate the effect of CO on alveolar-epithelial permeability, a radio-active labelled isotope, 51Cr-EDTA (MW 377), was instilled into the airways of rabbits. Subsequent egress of the marker from the lungs into arterial blood was determined in serial arterial blood samples. The 51Cr-EDTA counts increased significantly within 15 minutes in the CO-exposed animals, compared with the control animals, while dynamic lung compliance fell, airways resistance rose, and arterial blood pressure decreased. Ultrastructural study of the lungs of CO-exposed animals revealed epithelial and endothelial cell swelling, in terstitial edema, and alveolar type II cells depleted of lamellar bodies. These findings support the possibility that carbon monoxide intoxication is associated with increased alveolar-epithelial permeability.
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PMID:Carbon monoxide effect on alveolar epithelial permeability. 677 82

Utilizing a fluid percussion device, we measured the physiological effects of brain trauma in cats exposed to controlled levels of injury. Concussive brain injury at 3-4 atm of intensity led to profound elevations of the mean systemic arterial blood pressure from 128 +/- 26 to 229 +/- 33 mmHg, left ventricular end-diastolic pressure from 4 +/- 2 to 24 +/- 15 mmHg, and pulmonary wedge pressures (PWP) from 5 +/- 3 to 27 +/- 17 mmHg and a relatively moderate increase in intracranial pressure (ICP) from 6 +/- 3 to 38 +/- 31 mmHg (all P < 0.001). Pulmonary edema was evidenced by a significant increase in lung tissue wet-to-dry weight ratios to 3.74 +/- 0.81 as compared with a control group of 2.29 +/- 0.23 (P < 0.001). There was poor correlation between wet-to-dry weight ratios and PWP. Approximately 60% of all spontaneously breathing animals become permanently apneic within 6 min after injury, while the remaining 40% developed transient apnea. Arterial O2 or CO2 pressure alterations, in contrast to pretreatment with phentolamine did not affect the hemodynamic or edemogenic response to trauma. Phentolamine did not block the apneic response or increase in ICP. Comparative studies using intravenous levarterenol without trauma produced responses similar to trauma. Concussive brain injury of 3-4 atm results in pulmonary edema, apnea, sympathetically mediated peripheral vasoconstriction and left ventricular failure effect.
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PMID:Physiological effects of controlled concussive brain trauma. 677 80

Transcutaneous oxygen and carbon dioxide tensions (PtcO2 and PtcCO2) were compared with PaO2 and PaCO2 values in 9 patients with pulmonary edema due to acute myocardial infarction (AMI) measured during four experimental interventions: (a) intermittent mandatory ventilation (IMV) 4/min + PEEP0 (cm H2O); (b) intermittent positive pressure ventilation (IPPV)12 + PEEP0; (c) IMV4 + PEEP10; and (d) IPPV12 + PEEP10. PtcO2 responded rapidly to the institution of PEEP, the rise correlating well with that in PaO2 both on IMV4 (r = 0.78) and IPPV12 (r = 0.87). On the other hand, correlations between PtcO2 vs CI and PvO2 were poor (r being 0.45 and 0.24, respectively). Transcutaneous oxygen electrode is, thus, useful in monitoring patients with post-AMI pulmonary edema, as it rapidly reflects the effects of ventilatory therapy. A nonheated PtcCO2 sensor was used in 6 patients and a heated electrode in 3 patients. With the nonheated electrode, the correlation between PaCO2 and PtcCo2 was good (r = 0.86) in 5 patients, while r in the 3 patients with the heated electrode was 0.73. One patient having a cardiac index of 1.6 L/min . M2 showed a dissociation in PCO2 values. While PaCO2 remained unchanged, PtcCO2 rose to 73 torr and within some minutes the patient had asystole. PtcCO2 tension generally shows good correlation with PaCO2 and, thus, reflects ventilation. It may also prove to be useful in the early detection of critical low cardiac output states.
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PMID:Ventilatory pattern in respiratory failure arising from acute myocardial infarction. II. PtcO2 and PtcCO2 compared to Pao2 and PaCO2 during IMV4 vs IPPV12 and PEEP0 vs PEEP10. 680 Jun 99

The ventilatory response in acute lactic acidosis was assessed in 39 patients. In 18 patients, the acidosis was associated with phenformin ingestion and in 21, with other causes such as shock and sepsis, but not pulmonary edema. Arterial blood CO2 tensions and plasma bicarbonate concentrations were compared to those previously found in patients with uncomplicated diabetic ketoacidosis. In most of the lactic acidosis patients, arterial blood CO2 fell within the 95% confidence band calculated from the data in the ketoacidotic patients. Only 1 lactic acidotic patient had a triflingly lower CO2 tension. Shock was present in 8 of the 9 lactic acidotic patients whose CO2 tensions were more than 2 torr above the 95% confidence band.
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PMID:Ventilatory response in patients with acute lactic acidosis. 680 Jul 2


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