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PubMed1978

Qualitative detection of placidyl (ethchlorvynol) alone or in combination with poly-drugs in drug abuse urine screening programs using ion-exchange paper and/or liquid-liquid extraction.

Two procedures for the detection of ethchlorvynol are presented. Procedure I involves the use of SA-2-cation-exchange resin loaded paper. The use of multiple ion-exchange resin papers is proposed in a sequence that enables the detection of amphetamines, barbiturates, phenothiazines, propoxyphene (Darvon), phencyclidine, cocaine (benzoyl ecgonine), pentazocine (Talwin) and benzodiazepines in addition to ethchlorvynol. This procedure discusses the details of detecting ethchlorvynol in combination with the entire array of drugs of abuse depending on the needs of a clinical program. Procedure II involves the principle of liquid-liquid extraction using either raw or spent urines.

Chromatography, Ion Exchange↗
PubMed1987

Ethchlorvynol-induced pulmonary edema: a chronically instrumented, awake sheep model mimicking human disease.

Ethchlorvynol injection in humans leads to a clinical picture consistent with increased permeability pulmonary edema, ie, the adult respiratory distress syndrome. There has been only one such case reported in which the pulmonary wedge pressure was measured. In an attempt to mimic the human disease, the authors established the awake, unanesthetized chronic sheep lung lymph fistula model and injected 15 mg/kg of ethchlorvynol intravenously after a baseline period. There were transient increases in pulmonary artery and systemic blood pressure with decreases in cardiac output. Lymph flow increased five-fold and remained elevated for 24 hr, returning to normal by 48 hr. All animals survived. Pulmonary morphologic changes consisted of alveolar and interstitial edema and some disruption of endothelial and epithelial cells. These findings resolved by 48 hr postinjection. The authors conclude that this model mimics the findings in humans who have injected ethchlorvynol intravenously.

Animals↗
PubMed1980

Histamine receptor and prostaglandin synthetase blockers in ethchlorvynol-induced pulmonary edema in canines.

The injection of ethchlorvynol intravenously in humans and animals causes an increased permeability form of pulmonary edema. The proximate cause for this increased alveolar capillary membrane permeability is unknown but humoral mediators such as histamine and prostaglandins could play a role. To determine whether these agents were a factor in the altered permeability, we employed the saline-filled dog lung model and measured the flux of albumin across the alveolar capillary membrane. Following the intravenous injection of ethchlorvynol, there was a marked increase in permeability which was not altered by treatment with H1 and H2 receptor blockers or a prostaglandin synthetase inhibitor. We conclude that histamine and prostaglandins play no role in the increased permeability associated with ethchlorvynol injection.

Albumins↗
PubMed1989

Body distribution of ethchlorvynol.

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.

Adult↗
PubMed1983

Quantitative analysis of ethchlorvynol in a capsule dosage form by NMR spectroscopy.

A quantitative 1H-NMR procedure is described for measuring ethchlorvynol in capsules. Deuterochloroform is used as the solvent, and hexamethylenetetramine as the internal standard; the analysis is based on the comparison of the area of the AB peak system of ethchlorvynol with the area of the hexamethylenetetramine singlet. The 1H-NMR method yields results that are precise to within 1% and agree well with results of the more cumbersome and less specific USP titrimetric procedure.

Capsules↗
PubMed1990

Ethchlorvynol overdose.

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.

Chemical Phenomena↗
PubMed1977

Rapid micro-method for the measurement of ethchlorvynol in blood plasma and in urine by gas-liquid chromatography.

A rapid gas-liquid chromatographic method has been developed for use in the measurement of the hypnotic drug ethchlorvynol in small (50 microliter) volumes of either blood plasma or urine. Neither solvent transfer nor evaporation steps are used in the procedure and sources of interference have proved to be minimal. The method has been applied primarily to the analysis of specimens obtained from patients who had ingested an overdose of this drug. However with slight modification, the technique may be used in the measurement of the plasma concentrations of ethchlorvynol attained during therapy.

Animals↗
PubMed1977

Ethchlorvynol intoxication.

Ethchlorvynol intoxication can be confusing because of the lack of correlation between blood levels of the drug and clinical status. In this case, the patient was in a coma for approximately one week although he had a blood level of ethchlorvynol (0.8 mg/100 ml) generally considered to be subtoxic.

Ethchlorvynol↗
PubMed1989

Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak.

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.

Acute Disease↗
PubMed1977

Preliminary report on the effects of totigestational exposure to ethchlorvynol.

Ethchlorvynol, a sedative-hypnotic drug used clinically since 1955, has recently been the subject of renewed interest primarily because of its chemical relationship to vinyl chloride. In our totigestational studies, sperm-positive female rats were given a daily dose of ethchlorvynol dissolved in olive oil for 21 consecutive days. The dams were allowed to deliver and their offspring were observed for alterations in development by monitoring a number of gross behavioral, histological and biochemical parameters at newborn, weanling, puberty, adult and geriatric stages. Gross development appeared normal at time of weaning: however, offspring of treated dams showed increased behavioral activity in addition to alterations in a number of clinical chemistry parameters. The dose-response seen with most of the parameters suggests that the changes are drug related. However, the clinical pathological significance has not been ascertained.

Animals↗
PubMed1976

Ethchlorvynol (Placidyl)-induced pulmonary edema.

Two patients experienced severe nonhemodynamic pulmonary edema following the intravenous injection of 25 and 40 mg/kg of body weight of ethchlorvynol (Placidyl). The pulmonary edema cleared rapidly. Injection of Placidyl (12 to 80 mg/kg of body weight) intravenously into dogs caused acute, severe, nonhemodynamic pulmonary edema (as evidenced by markedly elevated lung weights and microscopic evidence of intra-alveolar edema), hypotension with a relative bradycardia, and a decreased cardiac output. Injection of polyethylene glycol, the vehicle in which ethchlorvynol is diluted, did not reproduce the syndrome.

Adult↗
PubMed1986

Acute urinary retention precipitated by ethchlorvynol overdose.

A 75-year-old woman developed acute urinary retention after ingestion of 20 100 mg ethchlorvynol tablets in a suicide attempt. To the authors' knowledge acute bladder dysfunction has not been previously ascribed to ethchlorvynol, but has been described often with therapy with various psychotropic medications. The mechanism of such bladder dysfunction may be direct action on bladder muscle, or parasympathetic cholinergic blockade, but has not been clarified. The risk of acute bladder dysfunction and the possibility of underlying bladder disorder must be considered in all patients receiving sedative-hypnotic drugs, particularly the elderly.

Aged↗
PubMed1966

Ethchlorvynol (Placidyl) intoxication and its treatment by hemodialysis.

Twenty hours after ingesting 15-25 g. of ethchlorvynol, a 37-year-old woman was admitted comatose and in shock. The blood level of ethchlorvynol was 21.6 mg. % (method of Wallace). Supportive measures were instituted and hemodialysis, carried out for 10 hours, removed 5.49 g. of the drug. The post-dialysis blood level was 9.05 mg. % and the rate of dialysance was 50.5 ml./min. Only 0.6 g. of the substance was recovered from the urine over the same period.Although dialysis removed significant amounts of the drug and sustained life, the patient remained comatose for five days before withdrawal symptoms and seizures developed.

Adult↗
PubMed1977

The effect of ethchlorvynol on pulmonary ultrastructure in dogs.

The ultrastructure of alveolar septae in dogs is investigated at times ranging from 30 seconds to 60 minutes after intravenous injection of ethchlorvynol (Placidyl). Pulmonary edematous fluid first appears in alveolar spaces 5 minutes after injection and becomes progressively more prominent with increasing time. Alveolar septae are initially somewhat fibrotic, and subsequently, most interstitial spaces become swollen and hydrated. Vesicles in endothelial cells increase with postinjectional time, and they seem to form channels or pores interconnecting capillaries and interstitial spaces. Similar vesicles in epithelial cells (Type 1) show an increase after 30 minutes, and they also seem to form channels or pores interconnecting interstitial spaces and the alveolus. Vesicles, whether in endothelial or epithelial cells, contain a flocculent filamentous material similar to plasma protein and the filamentous proteinaceous material in edematous fluid in alveolar spaces. Ethchlorvynol injection rapidly induces a non-hemodynamic form of pulmonary edema. Since cell junctions of both endothelial and epithelial cells remained intact, it is proposed that transalveolar transport of edematous proteinaceous fluid is mediated by means of endothelial and epithelial vesicles.

Animals↗
PubMedDate not supplied

Inhibition of nitric oxide synthesis improves arterial oxygenation in ethchlorvynol-induced acute lung injury in dogs.

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.

Animals↗
PubMed1978

Analysis of chlormethiazole, ethchlorvynol and trichloroethanol in biological fluids by gas-liquid chromatography as an aid to the diagnosis of acute poisoning.

A simple method has been developed whereby chlormethiazole, ethchlorvynol and trichloroethanol can be simultaneously detected and measured in biological fluids. The procedure is based upon the rapid extraction of a small (50-microliter) sample volume with an equal volume of chloroform containing an internal standard, followed by the gas-liquid chromatographic analysis of this extract. Specimens of blood plasma or serum, urine and gastric contents can be used, and no interference from either endogenous or exogenous sources has been observed. The method is suitable for the measurement of the plasma concentrations of these compounds attained after overdosage.

Chlormethiazole↗
PubMed1986

Indomethacin and ketanserin block ethchlorvynol-induced hypoxemia in dogs.

Intravenous injection of ethchlorvynol (ECV) leads to hypoxemia and a permeability pulmonary edema. Whether the hypoxemia is directly attributable to the pulmonary edema or caused by release of mediators has not been explored. Three groups of dogs were studied: (1) ECV, (2) indomethacin--ECV, and (3) ketanserin--ECV. In group 1, 25 to 30 mg/kg of ECV caused a significant fall in PaO2 at 4 min (92 +/- 12.6 to 77 +/- 21 mm Hg, p less than 0.05), which persisted throughout the experiment. The P(A-a)O2 gradient widened significantly at 3 min (22 +/- 11 to 31 +/- 16.8 mm Hg, p less than 0.05) and remained abnormal for the remainder of the experiment. There was no significant fall in PaO2 in groups 2 and 3. Lung tissue water to dry weight ratio increased significantly in all groups at 60 min. Lung tissue water to dry weight ratios were normal at 10 min after ECV injection in additional groups. It was concluded that ECV causes hypoxemia, which is mediated by cyclooxygenase products and 5 hydroxytryptamine. This hypoxemia can be prevented by the administration of drugs that block these products.

Animals↗