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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.

Ethchlorvynol (10 mg/kg) causes transient pulmonary hypertension and an increased permeability pulmonary edema in sheep. To determine the role of cyclooxygenase and its metabolites, histamine, and catecholamines in both phenomena, we studied five groups of sheep: group I, placebo; group II, ethchlorvynol; group III, indomethacin with ethchlorvynol; group IV, diphenhydramine with ethchlorvynol; group V, phentolamine with ethchlorvynol. Indomethacin, but not diphenhydramine or phentolamine, blunted the pulmonary hypertensive response seen immediately following the ethchlorvynol injection. However, none of the drugs had any effect on the increased permeability pulmonary edema. We conclude that cyclooxygenase or its metabolites partially mediates the hypertensive response but not the increased permeability pulmonary edema seen in sheep following ethchlorvynol injection.