Search

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.

We studied anesthetized dogs with right lymph duct (RLD) preparations and measured lymph flow, albumin concentrations in lymph (L) and plasma (P), pulmonary artery pressure (PAP), and pulmonary capillary wedge pressure (PCWP). Intravenous (iv) injection of ethchlorvynol (15-25 mg/kg) was followed by significant (p less than 0.02) increases in right lymph duct flow from 0.9 +/- 0.3 to 5.4 +/- 1.6 ml/h with stable PAP, PCWP, and L/P albumin (0.8 +/- 0.05 and 0.9 +/- 0.1). Similar results in RLD flow were obtained in dogs given 1) diphenhydramine, 3 mg/kg iv loading dose and 1.5 mg.kg-1 .h -1 infusion; 2) indomethacin, 4 gm/kg iv loading dose and 4 mg.kg-1h-1 infusion; 3) methylprednisolone, 30 mg/kg iv; 4) cyclophosphamide (40 mg/kg iv) to induce leukopenia (900 WBC/mm3) prior to ethchlorvynol injection. Cardiac lymph flow increased also and cardiac L/P albumin remained stable. Total hemolytic complement remained normal. We conclude that lung vascular permeability is increased following ethchlorvynol injection. Ethchlorvynol may have a direct effect on lung vascular permeability since, unlike other experimental models, complement activation, leukocytes, prostaglandins, and histamine play insignificant roles. A "final common pathway" may not exist for all forms of increased permeability pulmonary edema.