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)

The phenomenon called paradoxical undressing has been described from 33 cases of hypothermia collected from Swedish police reports. The cases were almost evenly distributed with regard to sex, age, and geographical distribution. The cases occurred more frequently in open land although cases from town areas were also found. Most incidents were recorded from November to February at low ambient temperatures, although cases were also reported at temperatures above 0 degree C. Arteriosclerosis and chronic alcoholism were important concomitant illnesses, the latter being frequent in middle-aged men. Epilepsy, diabetes, and pregnancy were present in single cases. Ethanol and other drugs were present in 67% of the males and in 78% of the females, ethanol predominating in men and various psychotropic agents in women. The mean blood ethanol concentration in males was 0.16% and in females, 0.18%. Most frequent findings at necropsy were purple spots or discoloration on the extremities, pulmonary edema, and gastric hemorrhages. It is concluded that paradoxical undressing might be explained by changes in peripheral vasoconstriction in the deeply hypothermic person. It represents the last effort of the victim and is followed almost immediately by unconsciousness and death.
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PMID:"Paradoxical undressing" in fatal hypothermia. 54 27

Since 1979, the potent narcotic analgesic fentanyl and its analogs have been synthesized in clandestine laboratories and sold as heroin substitutes. At least 112 overdose deaths have been associated with their use. In this study, toxicology data, autopsy findings, and coroners' investigative reports were reviewed in order to construct a profile of the typical fentanyl overdose victim and to identify any factors that might heighten the risk of death from fentanyl use. The "typical" fentanyl overdose victim was 32.5 +/- 6.7 years of age (range, 19 to 57 years), male (78%, compared with 22% female), and Caucasian (50%, compared with 29% Hispanic, 20% Black, and 0.9% Asian). With the exception of his or her age, the typical fentanyl overdose victim is quite similar to the typical heroin user. Nearly all the deaths (94%) occurred in California, yet within the state they were widely distributed throughout 17 counties and 44 cities. Pulmonary edema and congestion and needle puncture sites were consistent postmortem findings. No preexisting medical conditions were identified as possible risk factors. Although most of the fentanyl victims had a prior history of intravenous drug use, morphine or codeine were not commonly found, which suggests that the victims had little or no opiate tolerance. Ethanol was present in 38% of the cases and is thought to be a significant risk factor. Mean fentanyl concentrations in the body fluids were quite low: 3.0 +/- 3.1 ng/mL (0.3 +/- 0.31 micrograms/dL) in blood and 3.9 +/- 4.3 ng/mL (0.39 +/- 0.43 micrograms/dL) in urine, measured by radioimmunoassay. Although the potency of the analogs and the purity of street samples varies considerably, it is probably the general availability of the drug rather than the potency of a particular analog that determines the incidence of overdose deaths.
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PMID:Fentanyl-related deaths: demographics, circumstances, and toxicology of 112 cases. 206 23

Ethanol is a pulmonary vasoconstrictor in rat lungs perfused in situ with Krebs-Henseleit salt solution. Pentobarbital-anesthetized rats were tracheotomized, and an in situ recirculating isolated lung perfusion was instituted using a Krebs-Henseleit buffer with 3% bovine albumin at 37 degrees C. Changes in pulmonary arterial pressure and tracheal inspiratory pressure during intravenous ethanol infusion at four different cumulative doses were measured in normoxic (n = 6) and hyperoxic (n = 6) lungs, compared to normoxic perfusate (no ethanol infusion) controls (n = 6). Perfusate alcohol levels progressively increased in experimental groups. Perfusate gas and pH values were normal and not altered by ethanol. PAP increased by the end of ethanol infusion from 9.7 +/- 2 to 26 +/- 13 mm Hg in the normoxic group and from 10.6 to 22 +/- 9 mm Hg in the hyperoxic lungs (p less than .02); no change occurred in control lungs. Severe pulmonary edema occurred in 83% of the ethanol exposed lungs (vs. 0% of perfusate controls). Postethanol wet/dry weight ratios were twice normal (p less than .02). Pulmonary arterial pressure rose in two stages. First there was a 25-100% increase before airway pressure increased, representing pulmonary vasoconstriction. This was followed by a precipitous 100-500% transmitted pressure rise as severe pulmonary edema developed. Thus, we conclude that the vasoconstrictor effect of ethanol on the pulmonary circulation occurs in rats as well as in lambs, dogs, and humans. In isolated perfused rat lungs, the response is locally mediated.
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PMID:Ethanol induces acute pulmonary vasoconstriction in salt-perfused rat lungs. 274 52

A 34-year-old housewife with alcohol dependence vomited severely, lost consciousness, and died after she took more than 20 ml of 1% calcium cyanamide, and alcoholic beverage containing about 129 g of ethyl alcohol. An autopsy was performed around 16 h after death. The body weighed 55.5 kg, and moderate lung edema was found. Ethanol concentrations were 4.24 mg/g in the left heart blood, 4.39 mg/g in the right heart blood, and 21.55 mg/g in the stomach contents. Cyanamide concentrations were 0.63 microgram/g in the left heart blood, 0.20 microgram/g in the right heart blood, and 0.22 microgram/g in the stomach contents. The cause of death was determined to be acute ethanol intoxication with alcohol-cyanamide reaction.
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PMID:A fatal case of drinking and cyanamide intake. 918 22

Chronic alcohol abuse increases the incidence and mortality of the acute respiratory distress syndrome (ARDS) in septic patients. To examine a potential mechanism, we hypothesized that ethanol ingestion predisposes to sepsis-mediated acute lung injury by decreasing alveolar type II cell glutathione homeostasis and function. Lungs isolated from rats fed ethanol (20% in water for >/= 3 wk), compared with lungs from control-fed rats, had greater (P < 0. 05) edematous injury (reflected by nonhydrostatic weight gain) after endotoxin (2 mg/kg intraperitoneally) and subsequent perfusion ex vivo with n-formylmethionylleucylphenylalanine (fMLP, 10(-7) M). Ethanol ingestion decreased (P < 0.05) glutathione levels in the plasma, lung tissue, and lung lavage fluid, and increased (P < 0.05) oxidized glutathione levels in the lung lavage fluid. Furthermore, ethanol ingestion decreased type II cell glutathione content by 95% (P < 0.05), decreased (P < 0.05) type II cell surfactant synthesis and secretion, and decreased (P < 0.05) type II cell viability, in vitro. Finally, treatment with the glutathione precursors S-adenosyl-L-methionine and N-acetylcysteine in the final week of ethanol ingestion significantly reduced lung edema during perfusion ex vivo. We conclude that ethanol ingestion in rats alters alveolar type II cell glutathione levels and function, thereby predisposing the lung to acute edematous injury after endotoxemia. We speculate that chronic alcohol abuse in humans predisposes to ARDS through similar mechanisms.
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PMID:Chronic ethanol ingestion impairs alveolar type II cell glutathione homeostasis and function and predisposes to endotoxin-mediated acute edematous lung injury in rats. 946 70

Previously we reported that alcohol abuse increases the incidence of the acute respiratory distress syndrome (ARDS) in septic patients, and that chronic ethanol ingestion in rats depletes alveolar epithelial glutathione and increases endotoxin-mediated lung edema. In this study we examined a potential mechanism by which ethanol-induced glutathione depletion could predispose to acute lung injury. We hypothesized that glutathione depletion activates matrix metalloproteinases (MMPs), thereby increasing degradation of the alveolar extracellular matrix (ECM) during sepsis. Ethanol-fed rats (20% vol/vol in water for 6 wk) were given endotoxin (2 mg/kg, intraperitoneally) followed 2 h later by lung isolation and ex vivo perfusion with n-formyl-methionyl-leucyl-phenylalanine (fMLP) (10(-)(7) M). Ethanol ingestion increased (p < 0.05) MMP-9 and MMP-2 activity, as determined by zymography, in the lung tissue and lavage fluid compared with control-fed rats, and increased (p < 0.05) levels of the 7S fragment of type IV collagen in the lung lavage fluid. Ethanol ingestion increased activation, but not production, of the MMP-9 and MMP-2 zymogens. Finally, although concomitant ingestion of N-acetylcysteine had no effect (p > 0.05) on MMP production, it increased (p > 0.05) lung glutathione levels, blocked (p < 0.05) MMP-9 and MMP-2 activation, and decreased (p < 0.05) levels of the 7S fragment of type IV collagen. We conclude that chronic ethanol ingestion, via glutathione depletion, activates MMPs during sepsis, thereby increasing degradation of the alveolar epithelial ECM. Lois M, Brown LAS, Moss IM, Roman J, Guidot DM. Ethanol ingestion increases activation of matrix metalloproteinases in rat lungs during acute endotoxemia.
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PMID:Ethanol ingestion increases activation of matrix metalloproteinases in rat lungs during acute endotoxemia. 1050 28

Alcohol abuse markedly increases the risk of sepsis-mediated acute lung injury. In a rat model, ethanol ingestion alone (in the absence of any other stress) causes pulmonary glutathione depletion, increased expression of transforming growth factor-beta1 (TGF-beta1), and alveolar epithelial barrier dysfunction, even though the lung appears grossly normal. However, during endotoxemia, ethanol-fed rats release more activated TGF-beta1 into the alveolar space where it can exacerbate epithelial barrier dysfunction and lung edema. Ethanol ingestion activates the renin-angiotensin system, and angiotensin II is capable of inducing oxidative stress and TGF-beta1 expression. We determined that lisinopril, an angiotensin-converting enzyme inhibitor that decreases angiotensin II formation, limited lung glutathione depletion, and treatment with either lisinopril or losartan, a selective angiotensin II type 1 receptor blocker, normalized TGF-beta1 expression. The glutathione precursor procysteine also prevented TGF-beta1 expression, suggesting that TGF-beta1 may be induced indirectly by angiotensin II-mediated oxidative stress and glutathione depletion. Importantly, lisinopril treatment normalized barrier function in alveolar epithelial cell monolayers from ethanol-fed rats, and treatment with either lisinopril or losartan normalized alveolar epithelial barrier function in ethanol-fed rats in vivo, as reflected by lung liquid clearance of an intratracheal saline challenge, even during endotoxemia. In parallel, lisinopril treatment limited TGF-beta1 protein release into the alveolar space during endotoxemia. Together, these results suggest that angiotensin II mediates oxidative stress and the consequent TGF-beta1 expression and alveolar epithelial barrier dysfunction that characterize the alcoholic lung.
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PMID:Angiotensin II mediates glutathione depletion, transforming growth factor-beta1 expression, and epithelial barrier dysfunction in the alcoholic rat lung. 1590 76

Ethiofencarb is one of the carbamate compounds, which are, in general, less toxic than organophosphorus insecticides. This is due to their reversible acetylcholinesterase inhibition and relative inability to cross the blood-brain barrier. Generally, ethiofencarb is regarded to be of low toxicity (LD(50) > 200 mg/kg); however, severe poisoning and death are not uncommon. To our knowledge, no measurements of ethiofencarb and its metabolites in human postmortem whole blood have been published. We present here a case report of fatal ethiofencarb intoxication with quantitative analysis of ethiofencarb and its metabolites in ante- and postmortem blood. In addition, postmortem urine was collected and analyzed. A 56-year-old man, who worked as a gardener, was found in poor condition, sitting in his car seat. He had been vomiting. The man was admitted to the local hospital about 1 h later. At admission, he was conscious, but unable to speak clearly. His condition deteriorated, and he developed severe pulmonary edema. Resuscitation with atropine and adrenaline were attempted, but he died approximately 3 h after admission. The analysis of postmortem peripheral blood revealed 0.12 g/100 mL ethanol, 26.4 mg/L ethiofencarb, 37.9 mg/L ethiofencarbsulfoxide, and 0.9 mg/L ethiofencarbsulfone. Ethanol (0.26 g/100 mL), ethiofencarb, ethiofencarbsulfoxide, and ethiofencarbsulfone were also detected in urine.
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PMID:Lethal poisoning with ethiofencarb and ethanol. 1979 10