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The Western Journal of Medicine Feb 1974
Topics: Adult; Coma; Diagnosis, Differential; Ethchlorvynol; Eye Movements; Humans; Male; Medical History Taking; Neurologic Examination; Physical Examination; Pupil; Vestibule, Labyrinth
PubMed: 4544356
DOI: No ID Found -
British Medical Journal Jan 1963
Topics: Ethchlorvynol; Hypnotics and Sedatives
PubMed: 14018847
DOI: 10.1136/bmj.1.5325.262 -
Canadian Medical Association Journal Aug 1964A double-blind study with a Latin-square design was undertaken on 25 elderly patients, using a placebo and four hypnotic drugs: ethchlorvynol 500 mg., glutethimide 500...
A double-blind study with a Latin-square design was undertaken on 25 elderly patients, using a placebo and four hypnotic drugs: ethchlorvynol 500 mg., glutethimide 500 mg., chloral hydrate 500 mg., and secobarbital sodium 100 mg. The trial lasted for five weeks. The drugs were all effective compared with the placebo, differences in sleeping time being statistically significant. Differences between these four drugs were not statistically significant. Sleep was induced soonest by secobarbital and ethchlorvynol. Ethchlorvynol and glutethimide had a relatively somewhat longer period of activity than the others. Glutethimide produced most side effects, especially morning drowsiness. Ethchlorvynol and chloral hydrate produced relatively few cases of drowsiness.
Topics: Aged; Biomedical Research; Chloral Hydrate; Double-Blind Method; Drug Therapy; Ethchlorvynol; Geriatrics; Glutethimide; Humans; Hypnotics and Sedatives; Placebos; Secobarbital; Sleep; Toxicology
PubMed: 14179064
DOI: No ID Found -
Canadian Medical Association Journal Sep 1979The term addictive as used by the popular press frequently confuses the more precise concepts of acute and chronic tolerance, physical dependence and withdrawal, and...
The term addictive as used by the popular press frequently confuses the more precise concepts of acute and chronic tolerance, physical dependence and withdrawal, and psychologic dependence. Serious physical dependence on psychoactive drugs is rare and is easily managed. In contrast, psychologic dependence, the most important reason for persistent drug use, is much more common and is difficult to treat. Some tactics are available - for example, confrontation and discussion with the patient about how a drug is not going to be effective over long periods. Treating the symptom of a complex problem should, of course, not be expected to solve the problem. The most important tactic is to prescribe dependence-associated drugs only when clearly indicated, when the problem is responsive to drug therapy and for the shortest period necessary, without the option for renewing the prescription. Many problems related to drug use long after the period of expected benefit is past can be avoided by far more restrictive drug prescribing. Barbiturates and nonbarbiturate sedative hypnotics (e.g., ethchlorvynol, glutethimide, meprobamate, methaqualone and methyprylon) should not be prescribed for insomnia, acute reactive anxiety, chronic anxiety neurosis or depressive illnesses, since the safer and equally effective benzodiazepines, which are less associated with dependence, are available.
Topics: Amphetamines; Analgesics; Analgesics, Opioid; Barbiturates; Benzodiazepines; Humans; Hypnotics and Sedatives; Substance Withdrawal Syndrome; Substance-Related Disorders
PubMed: 42479
DOI: No ID Found -
Canadian Medical Association Journal Oct 1962The comparative sleep-inducing and sleep-sustaining effects of glutethimide, 0.5 g., and ethchlorvynol, 0.5 g., were studied in 20 patients hospitalized for a...
The comparative sleep-inducing and sleep-sustaining effects of glutethimide, 0.5 g., and ethchlorvynol, 0.5 g., were studied in 20 patients hospitalized for a considerable time (average: 21 years; minimum nine years and maximum 32 years) and not receiving psychotropic agents. Assessment of sleep and para-sleep parameters (pre-sleep tension; frequency of awakening at night; post-sleep activity) revealed that patients fell asleep faster (P>.001) and slept for a longer time with ethchlorvynol than with glutethimide.
Topics: Ethchlorvynol; Glutethimide; Humans; Hypnotics and Sedatives; Sleep; Sleep Initiation and Maintenance Disorders
PubMed: 13966278
DOI: No ID Found -
The American Journal of Pathology Jul 1988To determine the relationship among endothelial cell (EC) retraction, cell adenosine triphosphate (ATP), and the status of cellular actin, ATP levels, F-actin content,...
To determine the relationship among endothelial cell (EC) retraction, cell adenosine triphosphate (ATP), and the status of cellular actin, ATP levels, F-actin content, and cytochemical redistribution in bovine pulmonary artery endothelial cells were assessed. EC monolayers 7 days after confluence were exposed to ethchlorvynol (ECV), histamine, or cytochalasin B (cyto B) for time intervals from 5-90 minutes. All 3 agents resulted in endothelial cell retraction without significant effect on cellular ATP content. Sixty-minute incubation of monolayers in glucose-free media containing antimycin A and 2-deoxyglucose depleted cellular ATP to less than 10% of control levels. ATP depleted monolayers failed to retract when incubated with ECV, histamine, or cyto B. ATP depletion resulted in loss of the prominent EC margins but only a rare gap between adjacent cells. When ATP levels were allowed to recover, the ability of EC monolayers to retract was restored. Actin filaments in control monolayers localized to a dense peripheral band of actin, a paranuclear complex, and bundles of microfilaments orientated parallel to the long axis of the cell. ECV induced complete loss of the dense peripheral band and other changes in the actin disposition. Monolayers exposed to histamine showed a retraction of the dense peripheral band of actin to a subcortical position. Cyto B caused loss of the dense peripheral band and the longitudinal microfilament bundles. Monolayers depleted of ATP lost their dense peripheral band and exhibited a disorganized, tangled web of microfilaments. Neither histamine nor ECV modified the actin distribution in ATP-depleted monolayers, whereas exposure to cyto B resulted in substantial change in actin with formation of a rim inside the cell membrane and considerable loss of actin filaments. ECV or histamine induced a small reduction in F-actin content while cyto B resulted in a 50% decline in 15 minutes. ATP depletion resulted in a 19% decrease in F-actin, with no further reduction on subsequent exposure to histamine or ECV. Cyto B treatment of ATP-depleted monolayers caused a drop in F-actin content equivalent to that observed in cells with normal ATP levels. These studies indicate that ATP is essential for changes in actin filament distribution and endothelial cell retraction produced by ECV, histamine or cyto B, and make it unlikely that any of these agents acts simply by depolymerization of actin filaments or modification of the dense peripheral band, although disruption of the dense peripheral band may facilitate retraction in the presence of adequate levels of cell ATP.
Topics: Actins; Adenosine Triphosphate; Animals; Cell Line; Cytochalasin B; Endothelium, Vascular; Ethchlorvynol; Histamine
PubMed: 3394800
DOI: No ID Found -
The American Journal of Pathology Jun 1988Results of studies utilizing bronchoalveolar lavage (BAL) have led workers to propose that the neutrophil serves as the pivotal cellular element responsible for...
Results of studies utilizing bronchoalveolar lavage (BAL) have led workers to propose that the neutrophil serves as the pivotal cellular element responsible for promoting enhanced alveolar capillary membrane (ACM) permeability in certain forms of acute lung injury. The authors performed BAL on anesthetized, intubated, instrumented sheep before and after the administration of 15 mg/kg ethchlorvynol, a known pulmonary edemagenic agent. Bronchoalveolar lavage fluid (BALF) protein content increased from 0.62 +/- 0.05 to 1.5 +/- 0.15 mg/ml, and the percentage of neutrophils recovered from 2% +/- 1% at baseline to 35% +/- 7% (P less than 0.01) 60 minutes after infusion of ethchlorvynol. After ethchlorvynol infusion into neutropenic sheep (less than 500 cells/microliter), BALF protein content increased from 0.35 +/- 0.08 to 1.5 +/- 0.69 mg/ml (P less than 0.01) with no increase in BALF neutrophil count. In 3 non-neutropenic sheep BAL was performed at 15 and 30 minutes after ethchlorvynol infusion. BALF protein content increased significantly within 15 minutes, whereas the percentage of neutrophils did not change. These findings suggest coexistent ACM injury as reflected by increases in BALF protein content and increased number of neutrophils in BALF does not necessarily imply a cause-and-effect relationship in certain forms of acute lung injury.
Topics: Acute Disease; Animals; Bronchoalveolar Lavage Fluid; Capillary Permeability; Cell Movement; Disease Models, Animal; Ethchlorvynol; Hemodynamics; Lung Diseases; Neutrophils; Time Factors
PubMed: 3381875
DOI: No ID Found -
British Journal of Pharmacology and... Feb 1965
Topics: Barbiturates; Carbon Dioxide; Ethchlorvynol; Hypnotics and Sedatives; Hypoxia; Mathematics; Organophosphates; Pharmacology; Respiration; Respiratory Function Tests
PubMed: 14302355
DOI: 10.1111/j.1476-5381.1965.tb02097.x -
The American Journal of Pathology Jun 1985Ethchlorvynol (ECV), an agent which produces reversible pulmonary edema, was studied for its effects on cultured bovine pulmonary artery endothelial cell (BPAE) and...
Ethchlorvynol (ECV), an agent which produces reversible pulmonary edema, was studied for its effects on cultured bovine pulmonary artery endothelial cell (BPAE) and human umbilical vein endothelial cell (HUVE) monolayers. Endothelial cell monolayers 6 days post-confluent were treated with 1 mg/ml ECV for time intervals of from 5 minutes to 15 hours. ECV treatment caused a mild endothelial cell retraction evident at 10 minutes which increased in severity with increasing duration of exposure to ECV. Retraction of endothelial cells resulted in the formation of irregularly delineated gaps between cells, which remained attached to one another by slender filamentous processes. Despite the severity of the endothelial cell lesion, no cell lysis or cell detachment from the substratum occurred. Furthermore, removal of ECV from cell cultures resulted in the reversal of the endothelial cell lesion. Cytochemical distribution of actin microfilaments in control monolayers localized to a dense peripheral band of actin filaments and to a set of interconnected central microfilaments oriented in general parallel to the long axis of the cell. Endothelial cells treated with ECV for as little as 10 minutes showed a loss of F-actin from the dense peripheral band of microfilaments progressing until the dense peripheral band was entirely lost after 4 hours' exposure to ECV. By 4 hours central microfilaments had reorganized into a prominent series of microfilament bundles aligned parallel to each other and to the long axis of the cell. For investigation of a possible loss of attachment sites of actin filaments as the basis for the lesion, the localization of vinculin was examined in control and ECV-treated BPAE monolayers. After 2 hours' exposure to ECV, vinculin localization within monolayers was affected little, if at all. No effects of ECV on intermediate filaments were observed either. It is proposed that the dense peripheral band of actin bundles is important in maintaining well-spread endothelial cells in monolayers and that ECV acts to destroy the integrity of this structure. It is further proposed that a reaction of endothelial cells to ECV in vivo analogous to that seen in tissue culture accounts for the production of pulmonary edema by creating gaps between cells.
Topics: Animals; Capillary Permeability; Cattle; Cells, Cultured; Culture Techniques; Endothelium; Ethchlorvynol; Humans; Microscopy, Electron, Scanning; Pulmonary Artery; Umbilical Veins
PubMed: 4014437
DOI: No ID Found -
The American Journal of Pathology Jun 1984Studies of ethchlorvynol (ECV)-induced pulmonary edema were undertaken for determination of the structural basis of increased microvascular permeability. Rats were... (Comparative Study)
Comparative Study
Studies of ethchlorvynol (ECV)-induced pulmonary edema were undertaken for determination of the structural basis of increased microvascular permeability. Rats were administered an intravenous bolus dose of 15 mg/kg ECV and killed at time intervals between 5 minutes and 72 hours. Oyster glycogen and ferritin were used as permeability probes for identification of the sites of altered microvascular permeability. Edema fluid containing ferritin begins to accumulate in the alveolar interstitium 10 minutes after EVC . Thirty minutes after ECV, marked intersitial edema fluid is present containing both permeability probes. The absence of any appreciable transendothelial movement of either probe via vesicles and the presence of open endothelial junctions led the authors to propose the latter as the principal determinant of the increase in permeability. In addition to open endothelial junctions, prominent subendothelial blebs occur. These blebs develop in an otherwise intact endothelium and increase in frequency and size with time following their appearance at 10 minutes. Ferritin and glycogen progressively accumulate within the blebs. At 15 minutes the concentration of ferritin in blebs appears to equal that in plasma, whereas glycogen is absent or sparsely present in a few blebs. At 60 minutes both permeability probes have become concentrated in the blebs. The mechanism of formation of the blebs and concentration in them of the permeability probes cannot yet be specified. The lesion caused by ECV is completely reversible, so that by 72 hours after ECV there is complete resolution of interstitial edema, disappearance of the subendothelial blebs, and closure of endothelial junctions. A small amount of exudate remaining in the alveoli is cleared by 72 hours.
Topics: Animals; Capillary Permeability; Dose-Response Relationship, Drug; Endothelium; Ethchlorvynol; Lung; Male; Microscopy, Electron; Pulmonary Edema; Rats; Rats, Inbred Strains; Time Factors
PubMed: 6731587
DOI: No ID Found