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)

Etomidate and the closely related metomidate are known to inhibit cortisol synthesis. We studied the influence of metomidate on hemodynamic performance and survival time of bacteremic pigs. Thirty pigs, 30.2 +/- 0.8 kg, were anesthetized with intravenous metomidate (2.5 mg.kg-1.h-1) plus ketamine (3.0 mg.kg-1.h-1), and were then mechanically ventilated. The animals were randomly allocated to three groups of 10 pigs each. Group A received an infusion of live Pseudomonas aeruginosa bacteria (2.5.10(9).kg-1.h-1 organisms until death), Group B additionally received a bolus of 1 mg.kg-1 cortisol (followed by an infusion of 0.1 mg.kg-1.h-1) starting 1 h prior to the bacterial infusion, and Group C served as anesthesia control without receiving bacteria or cortisol. The experiments in Group C were terminated after 10 h. In Group A the cortisol level was severely suppressed from the very beginning. The animals died of circulatory failure after 4.3 +/- 0.4 h. In contrast, Group B exhibited fairly stable hemodynamics, but the animals died due to pulmonary edema after 11.1 +/- 1.3 h. Cortisol deficiency in metomidate anesthetized pigs facilitates the development of circulatory failure in the course of Pseudomonas bacteremia, which does not occur if cortisol is infused to reconstitute a physiological level. However, this cortisol substitution did not prevent the development of pulmonary edema caused by Pseudomonas aeruginosa. Possible mechanisms of the deleterious effect of cortisol deficiency and implications in regard to the clinical use of metomidate/etomidate are discussed.
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PMID:Cortisol deficiency in metomidate anesthetized bacteremic pigs: results in circulatory failure--beneficial effect of cortisol substitution. 257 34

We studied the effect of free fatty acids (FFA) i.v. on alveolar lung surfactant content of rabbits. A FFA mixture was given in doses from 0.1 to 20 mg X kg-1 X min-1 during 15 min in seven different experimental series (n = 45). Disaturated phosphatidylcholine (DSPC) content in lung airway lavage fluid was measured as an index of alveolar surfactant pool. DSPC was significantly increased (p less than 0.05) by 86% in the series receiving 20 mg FFA X kg-1 X min-1 as compared to control values (means +/- SD: 4.4 +/- 1.1 mg DSPC X kg-1 body weight). Smaller doses of FFA did not change DSPC, but induced a dose-related pulmonary oedema. All the rabbits receiving 20 mg FFA X kg-1 X min-1 died before completion of the 15 min infusion; they were hypoxaemic, hyperventilated and had a decrease in lung compliance. Hydrocortisone (20 mg X kg-1 i.v.) and methylprednisolone (30 mg X kg-1 i.v.) administered 2 h before FFA blocked the increase of DSPC induced by 20 mg FFA X kg-1 X min-1. Both drugs decreased pulmonary oedema and tended to normalize some of the pulmonary function indices, although they did not modify the lethality. In conclusion, acute i.v. infusion of FFA increased alveolar surfactant pool and produced pulmonary oedema; pretreatment with corticosteroids reduced these effects and protected the lung from some of the noxious effects of FFA.
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PMID:Effects of free fatty acid infusion on rabbit pulmonary surfactant. Influence of corticosteroids. 642 55

The effect of hydrocortisone on platelet activating factor (PAF)-induced pulmonary edema is studied. Thirty four isolated and perfused rabbit lung preparations were used: eight control preparations, eight PAF preparations with two doses of PAF called low dose (LD = 0.5 microg/kg of rabbit weight) and high dose (HD = 1 microg/kg of rabbit weight). Eighteen preparations divided in three groups of six were pretreated with doses of 20, 200 and 2000 mg of hydrocortisone and later given the same doses of PAF as described above. Hydrocortisone significantly decreased (P < 0.05) the effect of PAF LD over the pulmonary arterial pressure (Ppa) in the 200 and 2000 mg groups (58 and 89% decrease, respectively) and it significantly decreased (P < 0.05) the effect of PAF HD over Ppa in all hydrocortisone pretreated groups (48, 70 and 96% decrease, respectively). Fluid filtration rate (FFR) increases mediated by PAF HD were significantly inhibited (P < 0.05) in the 200 and 2000 mg groups (64 and 96% decrease, respectively). We conclude that hydrocortisone inhibits the effect of PAF over the pulmonary circulation.
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PMID:Effect of hydrocortisone on platelet activating factor induced lung edema in isolated rabbit lungs. 1078 45

A recent survey found that approximately 4% of very low birth weight infants in Japan were treated with glucocorticoids postnatally for circulatory collapse thought to be caused by late-onset adrenal insufficiency. We identified 11 preterm infants with clinical signs compatible with this diagnosis (hypotension, oliguria, hyponatremia, lung edema, and increased demand for oxygen treatment) and matched them for gestational age with 11 infants without such signs. Blood samples were obtained for cortisol and its precursors from the patient group before the administration of hydrocortisone, and from the control group during the same postnatal week. All samples were analyzed using a gas chromatography-mass spectrometry system. Cortisol concentrations did not differ between the two groups (6.6 +/- 4.5 vs 3.4 +/- 2.7 microg/dL); however, the total concentration of precursors in the pathway to cortisol production was significantly higher in the patient group (72.2 +/- 50.3 vs 25.0 +/- 28.5 microg/dL; p < 0.05). We conclude that the clinical picture of late-onset adrenal insufficiency in preterm infants is not a result of an absolute deficiency of cortisol production, but may be a result of a limited ability to synthesize sufficient cortisol for the degree of clinical stress.
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PMID:Comparison of serum cortisol concentrations in preterm infants with or without late-onset circulatory collapse due to adrenal insufficiency of prematurity. 1852 Mar 32