Ethchlorvynol chemical structure
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Ethchlorvynol

Ethchlorvynol is a sedative and hypnotic drug. It has been used to treat insomnia, but has been largely superseded and is only offered where an intolerance or allergy to other drugs exists. more...

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Along with expected sedative effects of relaxation and drowsiness ethchlorvynol can cause skin rashes, faintness, restlessness and euphoria. Early adjustment side effects can include nausea and vomiting, numbness, blurred vision, stomach pains and temporary dizziness. An overdose is marked by confusion, fever, peripheral numbness and weakness, reduced coordination and muscle control, slurred speech, reduced heartbeat.

It is addictive and after prolonged use can cause withdrawal symptoms including convulsions, hallucinations and memory loss. Due to these problems it is unusual for ethchlorvynol to be prescribed for periods exceeding seven days.

Ethchlorvynol is a member of the class of sedative-hypnotic tertiary carbinols such as methylparafynol. It is not a barbituric acid derivative. The systematic name of ethchlorvynol is usually given as ethyl 2-chlorovinyl ethynyl carbinol or 1-chloro-3-ethyl-1-penten-4-yl-3-ol. Its empirical formula is C7H9ClO. In the United States Abbott Laboratories used to sell it under the tradename Placidyl. Since Abbott and Banner Pharmacaps, which manufactured the generic version, discontinued production in 1999, ethchlorvynol is no longer available in the United States.

References and End Notes

  • PubChem Substance Summary: Ethchlorvynol National Center for Biotechnology Information. Accessed 1 September 2005 (UTC)
  • Electronic Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations Food and Drug Administration. Accessed 12 December 2005 (UTC)
  1. ^  Green List: Annex to the annual statistical report on psychotropic substances (form P) 23rd edition. August 2003. International Narcotics Board, Vienna International Centre. Accessed 1 September 2005 (UTC)

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What is the origin of pleural transudates and exudates? - Editorial
From CHEST, 9/1/92 by V. Courtney Broaddus

The classic teaching has been that pleural effusions arise from the pleural capillaries. Transudates were thought to result from an imbalance of the hydrostatic and osmotic forces in the pleural capillaries, leading to an increased flow of low-protein liquid into the pleural space, and exudates were thought to result from increased permeability of the capillaries in the pleura, leading to the accumulation of high-protein liquid in the pleural space. We now believe that this theory needs to be modified to include another common source of the liquid, namely: the interstitial space of the lungs.

In recent experimental and clinical studies involving hydrostatic pulmonary edema, transudates have been shown to arise from the interstitial space of the lung. When sheep were volume-loaded to cause lung edema, transudative liquid flowed across the visceral pleura of the isolated in situ lungs.[1] The pleural fluid contained the same protein concentration as did the lung lymph and the interstitial edema liquid in the lung. The volume of pleural fluid constituted about 25 percent of all edema liquid formed in the lung. In other experiments with high-pressure pulmonary edema in sheep, pleural fluid accumulated only after the development of pulmonary edema.[2] In patients with congestive heart failure, the presence of pleural effusions on ultrasound correlated more closely with the pulmonary venous pressure than with the systemic venous pressure; the likelihood of pleural effusions increased with the severity of pulmonary edema on chest radiographs.[3] Transudates associated with congestive heart failure therefore probably represent pulmonary edema liquid, and the pleural space may serve as another important route by which edema liquid clears the lung.

Exudates found in association with increased-permeability pulmonary edema probably also originate from the lung interstitium. When increased-permeability edema was induced in sheep by the infusion of oleic acid, pleural fluid accumulated only after pulmonary edema developed.[4] By morphologic study, there was no detectable injury to the visceral pleura. When pulmonary edema was induced by xylazine[5] or hyperoxia[6] in rats or by ethchlorvynol in sheep,[7] the investigators concluded that the high-protein pleural effusions arose from the parenchymal interstitial spaces of the lungs. By extension, we believe that when the lung is injured (eg, by pneumonia, pulmonary emboli, or lung transplantation), associated exudative pleural effusions probably also arise from the lung interstitium.

Should we still classify pleural effusions as transudates or exudates? To this we answer an unequivocal yes! The classification of the fluid as a transudate or an exudate will still indicate whether the fluid results from increased hydrostatic pressure or decreased osmotic pressure or from increased permeability. This will be a useful distinction whether the fluid arises from the pleura, the peritoneum, or, as is commonly the case, the lungs.

V. Courtney Broaddus, M.D. San Francisco; and Richard W. Light, M.D., F.C.C.P. Long Beach, California

References

[1] Broaddus VC, Wiener-Kronish JP, Staub NC. Clearance of lung edema into the pleural space of volume-loaded anesthetized sheep. J Appl Physiol 1990; 68:2623-30

[2] Allen S, Gabel J, Drake R. Left atrial hypertension causes pleural effusion formation in unanesthetized sheep. Am J Physiol 1989; 257(2 pt 2):H690-92

[3] Wiener-Kronish JP, Matthay MA, Callen PW, et al. Relationship of pleural effusions to pulmonary hemodynamics in patients with congestive heart failure. Am Rev Respir Dis 1985; 132:1253-56

[4] Wiener-Kronish JP, Broaddus VC, Albertine KH, Gropper MA, Matthay MA, Staub NC. Relationship of pleural effusions to increased permeability pulmonary edema in anesthetized sheep. J Clin Invest 1988; 82:1422-29

[5] Amouzadeh HR, Sangiah S, Qualls CW Jr, Cowell RL, Mauromoustakos A. Xylazine-induced pulmonary edema in rats. Toxicol Appl Pharmacol 1991; 108:417-27

[6] Bernaudin JF, Theven D, Pinchon MC, Brun-Pascaud M, Bellon B, Pocidalo JJ. Protein transfer in hyperoxic induced pleural effusion in the rat. Exp Lung Res 1986; 210:23-38

[7] Miller KS, Harley RA, Sahn SA. Pleural effusions associated with ethchlorvynol lung injury result from visceral pleural leak. Am Rev Respir Dis 1989; 140:764-78

COPYRIGHT 1992 American College of Chest Physicians
COPYRIGHT 2004 Gale Group

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