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1.
Clin Chest Med ; 25(1): 95-104, 2004 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15062601

RESUMO

Noncardiogenic pulmonary edema, and, to a lesser extent, acute respiratory distress syndrome (ARDS), are common clinical manifestations of drug-induced lung diseases. Clinical features and radiographic appearances are generally indistinguishable from other causes of pulmonary edema and ARDS. Typical manifestations include dyspnea, chest discomfort, tachypnea, and hypoxemia. Chest radiographs commonly reveal interstitial and alveolar filling infiltrates. Unlike pulmonary edema that is due to congestive heart failure, cardiomegaly and pulmonary vascular redistribution are generally absent in cases that are drug-related. Rare cases of drug-induced myocarditis with heart failure and pulmonary edema have been described. Results from laboratory evaluation and respiratory function tests are nonspecific.


Assuntos
Edema Pulmonar/induzido quimicamente , Síndrome do Desconforto Respiratório/induzido quimicamente , Antineoplásicos/efeitos adversos , Clorotiazida/efeitos adversos , Meios de Contraste , Diuréticos , Etclorvinol/efeitos adversos , Humanos , Hipnóticos e Sedativos/efeitos adversos , Doença Iatrogênica , Imunossupressores/efeitos adversos , Pulmão/efeitos dos fármacos , Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos , Tocolíticos/efeitos adversos , Tretinoína/efeitos adversos
3.
Am J Physiol ; 270(4 Pt 2): H1355-62, 1996 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8967376

RESUMO

The intravenous administration of ethchlorvynol (ECV), in dogs, resulted in an acute lung injury (ALI) characterized by a 200 +/- 80% increase in venous admixture and a 142 +/- 30% increase in extravascular lung water (EVLW). Pretreatment with the cytochrome P-450 inhibitor 8-methoxypsoralen prevented the ECV-induced increase in venous admixture but not the increased EVLW. These findings parallel those reported for cyclooxygenase inhibition in ECV-induced ALI and suggest that an arachidonic acid (AA) metabolite of pulmonary cytochrome P-450 activity may mediate the increase in venous admixture of ALI. We demonstrate that canine pulmonary microsomes metabolize [1-(14)C]AA to a variety of products, including the cytochrome P-450 metabolites 5,6-, 8,9-, 11,12-, and 14,15-epoxyeicosatrienoic acid (EET). In prostaglandin F2 alpha-contracted, isolated pulmonary venous rings, 5,6-EET induced relaxation in a concentration-dependent manner. This action of 5,6-EET was prevented by indomethacin (10(-5) M). These results suggest that may serve as the cyclooxygenase-dependent endogenous pulmonary vasodilator responsible for the increase in venous admixture of ECV-induced ALI.


Assuntos
Inibidores das Enzimas do Citocromo P-450 , Hipóxia/etiologia , Hipóxia/fisiopatologia , Lesão Pulmonar , Ácido 8,11,14-Eicosatrienoico/análogos & derivados , Ácido 8,11,14-Eicosatrienoico/metabolismo , Ácido 8,11,14-Eicosatrienoico/farmacologia , Animais , Dinoprosta/farmacologia , Cães , Etclorvinol/farmacologia , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Masculino , Metoxaleno/farmacologia , Microssomos/metabolismo , Veículos Farmacêuticos/farmacologia , Vasoconstrição/efeitos dos fármacos
4.
Pol J Pharmacol ; 47(5): 473-8, 1995.
Artigo em Inglês | MEDLINE | ID: mdl-8868143

RESUMO

In both humans and in experimental animals, acute lung injury (ALI) is characterized by the development of pulmonary edema and arterial hypoxemia. It has been reported that the hypoxemia of ALI is related to the failure of those mechanisms that result in the diversion of blood flow away from hypoxic (edematous) lung units to those that are well oxygenated. One such mechanism is hypoxic pulmonary vasoconstriction (HPV). In the pulmonary circulation, endogenous nitric oxide (NO) has been shown to oppose HPV and, thereby, to support blood flow to hypoxic alveoli. In the present work we investigated the hypothesis that, in ALI, endogenous NO, by virtue of its ability to oppose HPV, supports blood flow to hypoxic lung units resulting in increases in venous admixture (Qva/Qt) and decreases in arterial oxygen tension (PaO2). In anesthetized and mechanically ventilated dogs, the intravenous administration of ethchlorvynol (ECV, 15 mg/kg) resulted in an increase in extravascular lung water (EVLW) of 10 +/- 1 ml/kg body wt (p < 0.001) as well as a 120 +/- 45% increase in Qva/Qt (p < 0.01) and a 23 +/- 5% decrease in PaO2 (p < 0.01) (n = 3). L-NAME (1 mg/kg iv, followed by 5 mg/kg/h, iv), administrated 60 min after ethchlorvynol (ECV), prevented entirely the ECV-induced increase in Qva/Qt and fall in PaO2 with minimal effect on EVLW (n = 3). We conclude that, in this model of ALI, endogenous NO is present in the lung and acts to support blood flow to poorly oxygenated lung units resulting, thereby, in reductions in PaO2.


Assuntos
Inibidores Enzimáticos/uso terapêutico , Pneumopatias/metabolismo , NG-Nitroarginina Metil Éster/uso terapêutico , Óxido Nítrico Sintase/antagonistas & inibidores , Óxido Nítrico/biossíntese , Oxigênio/sangue , Animais , Gasometria , Cães , Etclorvinol , Água Extravascular Pulmonar/efeitos dos fármacos , Hemodinâmica/efeitos dos fármacos , Hipóxia/fisiopatologia , Pneumopatias/sangue , Pneumopatias/induzido quimicamente , Masculino
5.
Am Rev Respir Dis ; 148(4 Pt 1): 852-9, 1993 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-7692773

RESUMO

The efficacy of hydroxyethyl starch (HES) in limiting alveolar flooding after acute lung injury was investigated using ethchlorvynol (ECV)-induced low pressure pulmonary edema in dogs. Harvested autologous plasma (PL) (control, n = 8) or 6% HES (n = 8) was infused (25 ml/kg) along with packed cells to result in an isovolemic, normochromic preparation before the administration of ECV. Extravascular thermal volume significantly increased after ECV administration in both groups of animals (6.6 to 13.4 ml/kg in PL, 6.5 to 15.0 ml/kg in HES). Systemic arterial PO2 decreased from 216 +/- 4 to 113 +/- 20 mm Hg, and venous admixture increased from 2.8 to 12.8% in the PL group but was not significantly changed in the HES group (219 +/- 5 to 203 +/- 8 mm Hg, and 2.9 to 4.4%, respectively). Epithelial lining fluid volumes after ECV administration increased in both groups but were elevated in the PL group to a greater extent than in the HES group (13.5 ml in HES versus 24.8 ml in PL). In the HES group there appeared to be no difference in the ability of plasma proteins to move across the alveolar epithelium. These results suggest that HES attenuates the flooding of the alveolar space and the resulting alterations in gas exchange during the development of low pressure pulmonary edema. The replacement of the plasma proteins with HES and the apparent inability of HES to cross the epithelial barrier into the alveoli may account for the protective effect of HES in these experiments.


Assuntos
Derivados de Hidroxietil Amido/uso terapêutico , Alvéolos Pulmonares/efeitos dos fármacos , Edema Pulmonar/tratamento farmacológico , Doença Aguda , Análise de Variância , Animais , Gasometria , Líquido da Lavagem Broncoalveolar/química , Modelos Animais de Doenças , Cães , Avaliação Pré-Clínica de Medicamentos , Etclorvinol , Água Extravascular Pulmonar/efeitos dos fármacos , Modelos Lineares , Masculino , Troca Plasmática , Alvéolos Pulmonares/fisiopatologia , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/epidemiologia , Edema Pulmonar/fisiopatologia , Troca Gasosa Pulmonar/efeitos dos fármacos
6.
Acta Anaesthesiol Scand ; 37(2): 219-22, 1993 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-8447214

RESUMO

The effects of amrinone and CaCl2 on pulmonary vasculature and biventricular function in sheep with acute lung injury (ALI) were studied. Seven sheep were ventilated with a tidal volume of 10-12 ml.kg-1 with end-tidal CO2 of 40 +/- 5 mmHg (5.3 +/- 0.7 kPa) after acute lung injury was induced with up to 30 mg kg-1 of ethchlorvynol (ECV). Biventricular function and hemodynamic profiles were estimated with a rapid computerized thermodilution method and modified pulmonary artery catheters after acute lung injury, following a loading dose (1 mg kg-1) and maintenance dose (5 micrograms kg-1 min-1) of amrinone and after a bolus dose of CaCl2 (20 mg kg-1). ECV successfully induced acute lung damage in sheep, causing significant increases in pulmonary artery pressure (PAP) and pulmonary vascular resistance index (PVRI). Amrinone reversed the unfavorable changes induced by ECV, significantly reducing PAP, PVRI and left ventricular end-diastolic volume (LVEDV). CaCl2, however, reversed the effect of amrinone and increased PAP, PVRI, and LVEDV but decreased left ventricular ejection fraction.


Assuntos
Amrinona/farmacologia , Cloreto de Cálcio/farmacologia , Etclorvinol/efeitos adversos , Pulmão/irrigação sanguínea , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/fisiopatologia , Função Ventricular Esquerda/efeitos dos fármacos , Função Ventricular Direita/efeitos dos fármacos , Animais , Pressão Sanguínea/efeitos dos fármacos , Débito Cardíaco/efeitos dos fármacos , Volume Cardíaco/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Artéria Pulmonar , Pressão Propulsora Pulmonar/efeitos dos fármacos , Ovinos , Volume Sistólico/efeitos dos fármacos , Resistência Vascular/efeitos dos fármacos , Função Ventricular Esquerda/fisiologia , Função Ventricular Direita/fisiologia
7.
J Appl Physiol (1985) ; 73(1): 108-16, 1992 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-1506357

RESUMO

We examined the effects of positive end-expiratory pressure (PEEP) and tidal volume on the distribution of ventilation and perfusion in a canine model of asymmetric lung injury. Unilateral right lung edema was established in 10 animals by use of a selective infusion of ethchlorvynol. Five animals were tested in the supine position (horizontal asymmetry) and five in the right decubitus position (vertical asymmetry). Raising PEEP from 5 to 12 cmH2O improved oxygenation despite a redistribution of blood flow toward the damage lung and a consistent decrease in total respiratory system compliance. This improvement paralleled a redistribution of tidal ventilation to the injured lung. This was effected primarily by a fall in the compliance of the noninjured lung due to hyperinflation. The effects of higher tidal volume were additive to those of PEEP. We propose that the major effect of PEEP in inhomogeneous lung injury is to restore tidal ventilation to a population of alveoli recruitable only at high airway pressures.


Assuntos
Etclorvinol/toxicidade , Pneumopatias/fisiopatologia , Animais , Pressão Sanguínea/fisiologia , Cães , Hemodinâmica/efeitos dos fármacos , Intubação Intratraqueal , Complacência Pulmonar/fisiologia , Pneumopatias/induzido quimicamente , Respiração com Pressão Positiva , Edema Pulmonar/metabolismo , Edema Pulmonar/fisiopatologia , Troca Gasosa Pulmonar/efeitos dos fármacos , Volume de Ventilação Pulmonar/fisiologia
8.
J Appl Physiol (1985) ; 72(3): 1156-65, 1992 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-1568970

RESUMO

The role of cyclooxygenase products in acute lung injury was determined by pretreatment of dogs with ibuprofen before injury with intravenous ethchlovynol (ECV). In animals given ECV only, lung injury resulted in extravascular lung water of 18.9 ml/kg after 2 h, which was significantly higher than the 14.8 ml/kg in the group pretreated with ibuprofen. The comparison of gravimetric and indicator-dilution measurements of edema fluid indicates that edema fluid could not be reliably detected after treatment with ibuprofen because of diversion of flow from injured areas. Venous admixture increased from 6% at baseline to 32% 120 min after ECV in the vehicle-pretreated group compared with an increase from 4% at baseline to 7% in the ibuprofen-pretreated group. The regression analysis of the relationship between venous admixture and extravascular lung water indicated that, at any level of edema, venous admixture was significantly less in the group treated with ibuprofen than in the untreated group. Measurement of plasma and bronchoalveolar lavage fluid indicated that ibuprofen inhibited cyclooxygenase activity without affecting lipoxygenase activity. These results suggest that in intact dogs ibuprofen has a protective effect on both pulmonary gas transfer and pulmonary edema formation in ECV-injured lungs, which is consistent with limiting blood flow to injured segments of the lung.


Assuntos
Etclorvinol/antagonistas & inibidores , Ibuprofeno/farmacologia , Lesão Pulmonar , Animais , Cães , Eicosanoides/metabolismo , Etclorvinol/toxicidade , Pulmão/irrigação sanguínea , Pulmão/fisiopatologia , Masculino , Prostaglandina-Endoperóxido Sintases/metabolismo , Circulação Pulmonar/efeitos dos fármacos , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/fisiopatologia , Edema Pulmonar/prevenção & controle , Troca Gasosa Pulmonar/efeitos dos fármacos , Fluxo Sanguíneo Regional/efeitos dos fármacos
10.
J Appl Physiol (1985) ; 71(1): 43-9, 1991 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-1917763

RESUMO

The effect of three chemically dissimilar cyclooxygenase inhibitors on ethchlorvynol-(ECV) induced acute lung injury was studied in isolated buffer-perfused rat and blood-perfused rabbit lungs. ECV caused the microvascular fluid filtration coefficient (Kf) to increase by greater than threefold in the rat lungs and twofold in the rabbit lungs. ECV caused increased pulmonary vascular resistance (PVR) and microvascular pressure measured by the double occlusion technique (Pdo) compared with the vehicle control group in the rat experiments. However, ECV had no effect on PVR or Pdo in the rabbit experiments. Pretreatment with the cyclooxygenase inhibitors indomethacin, ibuprofen, and meclofenamate prevented the increase in microvascular permeability in both the rat and rabbit lung preparations. The cyclooxygenase inhibitors also prevented the ECV-induced PVR and Pdo increases in the rat lungs but had no effect on PVR or Pdo in the rabbit lungs. These results indicate that cyclooxygenase products of arachidonate metabolism mediate the ECV-induced Kf increase in both isolated rat and rabbit lungs.


Assuntos
Inibidores de Ciclo-Oxigenase/farmacologia , Etclorvinol/antagonistas & inibidores , Pneumopatias/prevenção & controle , Animais , Permeabilidade Capilar/efeitos dos fármacos , Etclorvinol/toxicidade , Ibuprofeno/farmacologia , Técnicas In Vitro , Indometacina/farmacologia , Pneumopatias/induzido quimicamente , Masculino , Ácido Meclofenâmico/farmacologia , Circulação Pulmonar/efeitos dos fármacos , Coelhos , Ratos , Ratos Endogâmicos , Resistência Vascular/efeitos dos fármacos
12.
J Anal Toxicol ; 14(6): 348-52, 1990.
Artigo em Inglês | MEDLINE | ID: mdl-2087094

RESUMO

Cases of nonfatal (51) and fatal (38) ingestions involving ethchlorvynol over a 14-year period (1975 through 1988) were reviewed in order to evaluate the current status of ingestion of this drug. In both series of cases men and women were involved approximately equally. Sixty-three percent of cases in both series occurred during the period 1975 through 1980. Most (78% of nonfatal and 89% of fatal) ingestions involved other drugs in addition to ethchlorvynol. Physical findings for nonfatal ingestions and causes of death for fatal ingestions are presented. Blood ethchlorvynol concentrations are discussed, and a composite of the average patient for each series is presented. Although ethchlorvynol abuse appears to be decreasing with time, it still occurs, and a search for this sedative-hypnotic agent should be included in the so-called "toxicology screen."


Assuntos
Etclorvinol/sangue , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , California/epidemiologia , Etclorvinol/envenenamento , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Envenenamento/epidemiologia
14.
Am J Emerg Med ; 8(3): 246-50, 1990 May.
Artigo em Inglês | MEDLINE | ID: mdl-2331266

RESUMO

Ethchlorvynol remains a drug that frequently surfaces in clinical emergency practice despite safer and more effective pharmaceutical agents on the market. Effects such as poisoning, dependence, ocular damage, and overdose continue to receive attention in the literature. Awareness of complications and treatment in ethchlorvynol exposure requires attention to a drug remaining clinically available without an appropriate clinical indication.


Assuntos
Overdose de Drogas/terapia , Emergências , Etclorvinol/efeitos adversos , Fenômenos Químicos , Química , Overdose de Drogas/diagnóstico , Overdose de Drogas/epidemiologia , Etclorvinol/farmacocinética , Etclorvinol/farmacologia , Hemoperfusão , Humanos , Intubação Gastrointestinal , Sucção , Estados Unidos/epidemiologia
15.
Crit Care Med ; 18(2): 208-12, 1990 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-2298014

RESUMO

In nine anesthetized and ventilated swine, a microcomputer calculated cardiac output, venous admixture (Qsp/Qt) and physiologic deadspace (VD/VT) every 20 sec, utilizing dual oximetry and a gas exchange analyzer. After lung injury with ethchlorvynol (ECV), animals were bled 40% blood volume over 40 min. Mean cardiac output decreased 7.0 to 2.2 L/min (p less than .05) accompanied by a decrease in mean Qsp/Qt from 0.28 to 0.14 (p less than .05) and an increase in mean VD/VT from 0.39 to 0.54 (p less than .05). Arterial Hgb saturation (Sao2) increased from 88 +/- 7% to 90 +/- 6%. On regression of all data points for each variable, Qsp/Qt had a positive correlation with cardiac output (r = .90), mean arterial pressure (MAP, r = .87), mean pulmonary artery pressure (MPAP, r = .86), and mixed venous Hgb saturation (Svo2, r = .89, p less than .001). VD/VT had an inverse correlation with cardiac output (r = -.90), MAP (r = -.82), Qsp/Qt (r = -.83), MPAP (r = -.77), and Svo2 (r = -.92, p less than .001). The decreasing Qsp/Qt and increasing VD/VT, with decreasing pulmonary perfusion pressures, were attributed to selective loss of perfusion to alveoli with low ventilation/perfusion ratios.


Assuntos
Pneumopatias/fisiopatologia , Choque/fisiopatologia , Animais , Etclorvinol/envenenamento , Pneumopatias/induzido quimicamente , Microcomputadores , Monitorização Fisiológica , Oximetria , Suínos
16.
Am Rev Respir Dis ; 140(3): 764-70, 1989 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-2782746

RESUMO

Traditional thinking suggests that pleural fluid develops on the basis of systemic venous hypertension or a primary pleural process. Recent investigations, however, indicate that both acute lung injury and pulmonary venous hypertension can be important in the pathogenesis of pleural effusions. To evaluate the role of acute lung injury in the formation of pleural effusions, we developed a model of acute, reversible lung injury in NZW rabbits. Intravenous ethchlorvynol (ECV), known to produce permeability edema in humans, was used to produce permeability pulmonary edema in rabbits. The injury was examined over 14 days with bronchoalveolar lavage, pleural fluid analysis, and morphologic analysis. Ethchlorvynol injection (40 mg/kg) produced a PMN-predominant, exudative alveolitis (2 h), alveolar hemorrhage (6 to 10 h), and pleural effusions by 2 h (peak, 10 h). Pathologic findings included a patchy, subpleural, hemorrhagic PMN inflammatory response, which peaked by 24 h, and an acute PMN vasculitis of small arterioles and capillaries; these changes resolved in 5 to 7 days. No parietal pleural abnormalities were observed. We conclude that ECV induces an acute, reversible parenchymal lung injury resulting in a capillary leak and that fluid moves from the interstitium of the lung into the pleural space along a pressure gradient through a relatively permeable mesothelium. The data support the concept that diffuse or localized lung injury can result in pleural effusions.


Assuntos
Etclorvinol/toxicidade , Pleura/fisiopatologia , Derrame Pleural/fisiopatologia , Doença Aguda , Animais , Líquido da Lavagem Broncoalveolar/citologia , Capilares/patologia , Pulmão/efeitos dos fármacos , Pulmão/patologia , Pulmão/fisiopatologia , Permeabilidade , Pleura/irrigação sanguínea , Pleura/patologia , Derrame Pleural/induzido quimicamente , Derrame Pleural/patologia , Edema Pulmonar/induzido quimicamente , Coelhos
17.
J Forensic Sci ; 34(3): 687-90, 1989 May.
Artigo em Inglês | MEDLINE | ID: mdl-2738567

RESUMO

Ethchlorvynol (Placidyl) is a nonbarbiturate sedative hypnotic. Two fatal cases of ethchlorvynol overdose are reported. Toxicological analyses of body fluids and tissues were performed by gas chromatography using a flame-ionization detector. The quantitative method was sensitive and reproducible. Body distribution of ethchlorvynol in blood and other tissues is presented. Biological samples analyzed included blood, urine, bile, liver, kidney, eye fluid, and gastric contents. Results presented add to the pharmacokinetic data needed to study the disposition of drugs in different tissues. Findings in present two cases are compared with published toxicological data.


Assuntos
Etclorvinol/envenenamento , Adulto , Líquidos Corporais/metabolismo , Etclorvinol/farmacocinética , Ionização de Chama , Humanos , Fígado/metabolismo , Masculino , Transtornos Relacionados ao Uso de Substâncias/metabolismo , Suicídio , Distribuição Tecidual
18.
Crit Care Med ; 17(3): 255-60, 1989 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-2493356

RESUMO

Although ethchlorvynol (ECV) has been used to induce pulmonary damage in animals, changes after injection of this drug have not been studied, nor has the stability of the animal been assessed after injection. Continuously monitored hemodynamic and respiratory changes were followed during and after iv injection of 55 mg/kg ECV in ethanol into anesthetized, paralyzed, and ventilated swine (n = 5) and compared to changes in a control group given ethanol alone (n = 5). Arterial and mixed venous saturations were measured by fiberoptic vascular catheters and oxygen exchange by a gas monitor. Twelve direct and derived variables were monitored every 20 sec using a computer data acquisition system. Arterial oxygen saturation was kept at 90 +/- 2% by adjustment of FIO2. Ethanol produced only transitory changes during infusion. Significant elevations in pulmonary vascular resistance (PVR), shunt (Qsp/Qt) and deadspace (VD/VT) were observed during and after ECV. These were unaccompanied by changes in cardiac output or arterial pressure. PVR increased by 137%, Qsp/Qt by 67%, and VD/VT by 28% over 30 min. These changes were then sustained in the postinfusion period, producing a stable model of early adult respiratory distress syndrome for 3.5 h.


Assuntos
Etclorvinol/efeitos adversos , Pulmão/efeitos dos fármacos , Síndrome do Desconforto Respiratório/induzido quimicamente , Animais , Pressão Sanguínea/efeitos dos fármacos , Dióxido de Carbono/sangue , Débito Cardíaco/efeitos dos fármacos , Cateterismo Venoso Central , Eletrocardiografia , Etanol/efeitos adversos , Frequência Cardíaca/efeitos dos fármacos , Oxigênio/sangue , Consumo de Oxigênio/efeitos dos fármacos , Espaço Morto Respiratório/efeitos dos fármacos , Síndrome do Desconforto Respiratório/fisiopatologia , Suínos , Resistência Vascular/efeitos dos fármacos
19.
Chest ; 95(2): 464-6, 1989 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-2914502

RESUMO

A 26-year-old man had bilateral alveolar infiltrates and exudative pleural effusions following self-administration of intravenous ethchlorvynol (ECV). The effusions and pulmonary edema resolved by 72 h with supportive therapy only. As no other etiology was established, we concluded that the pathogenesis of the pleural fluid was the transvisceral pleural leak of the increased extravascular lung water induced by ECV. Current experimental and clinical evidence support the concept that pleural effusions probably develop in most states of permeability pulmonary edema.


Assuntos
Etclorvinol , Derrame Pleural/induzido quimicamente , Transtornos Relacionados ao Uso de Substâncias/complicações , Adulto , Etclorvinol/administração & dosagem , Humanos , Injeções Intravenosas , Masculino , Derrame Pleural/diagnóstico por imagem , Edema Pulmonar/induzido quimicamente , Edema Pulmonar/diagnóstico por imagem , Radiografia
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