Chest
Volume 73, Issue 1, January 1978, Pages 75-78
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Experimental Approaches
The Role of Leukocytes in Ethchlorvynol-Induced Pulmonary Edema

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Intravenous administration of ethchlorvynol (Placidyl) is known to produce noncardiogenic pulmonary edema in animals and humans. Since intrapulmonary sequestration of leukocytes has been observed to occur following injection of ethchlorvynol, we evaluated the role of these elements of the blood in producing pulmonary edema. In vivo studies in dogs showed intrapulmonary trapping of leukocytes, as evidenced by increasing leukocyte differences between blood from the pulmonary artery and arterial blood. In both animals with normal leukocyte counts and those depleted of leukocytes (<500 cells per millimeter), pulmonary edema occurred, as evidenced by increased pulmonary water after injection of ethchlorvynol. Preparations of isolated lung perfused with either whole blood or leukocyte-poor plasma had similar gains in weight following injection of ethchlorvynol, in spite of marked differences in leukocyte counts. We conclude that intrapulmonary sequestered leukocytes do not play a role in ethchlorvynol-induced pulmonary edema.

Section snippets

In Vivo

Normal Dogs. Normal dogs were those not treated with cyclophosphamide (Cytoxan). Seven mongrel dogs were anesthetized with an intravenous injection of 30 mg of pentobarbital sodium per kilogram of body weight. The dogs were intubated and ventilated with a respirator (Harvard) at a fractional concentration of oxygen in the inspired gas (FIo2) of 1.0, and the following catheters were inserted: (1) a No. 7 Swan-Ganz catheter via the femoral vein into the pulmonary artery under pressure monitoring;

In Vivo Studies

Normal Dogs (Not Treated with Cyclophosphamide). Table 1 gives the total leukocyte counts of pulmonary arterial and arterial blood before and one, three, and five minutes after injection of ethchlorvynol. Prior to the injection of ethchlorvynol, the arterial leukocyte counts tended to be lower than those found in the pulmonary artery. Following injection of ethchlorvynol, the differences between pulmonary arterial blood and arterial blood increased markedly in all animals at all times of

Discussion

We became interested in the pulmonary edematogenic properties of ethchlorvynol after caring for two young patients who initially had respiratory insufficiency (adult respiratory distress syndrome) after the intravenous injection of this common oral sedative.9 Ongoing studies have revealed the following: intravenously administered ethchlorvynol accumulates in a passive fashion in pulmonary tissue within minutes of injection;10 the permeability of alveolar capillary membranes is markedly

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