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Monocrotaline, a plant alkaloid shown histologically to produce pulmonary endothelial damage and edema, was used in dogs to produce an acute model of noncardiogenic pulmonary edema. Following intravenous injection there was no change in pulmonary vascular pressures or heart rate; cardiac output fell and pulmonary vascular resistance increased. After 2 h measurement of lung water demonstrated modest pulmonary edema in all animals. The degree of edema produced was more consistent and reproducible than that following alloxan or alpha-naphthylthiourea.

A review of 180 cancer patients requiring mechanical ventilation disclosed that 26% survived to extubation, and 13% and 7% were alive at two and six months, respectively. Mortality was related to several factors individually and the cumulative number of organ systems dysfunctioning in a given patient. Compared with general intensive care patients, those with respiratory failure and neoplastic disease demonstrated a high incidence of drug-induced pulmonary disease, hematologic abnormalities, pneumothorax, and infections with multiple and unusual organisms--all of which alter the approach to management. Although the long-term survival was poor, immediate survival was comparable with that of many groups of patients with respiratory failure.

INCREASED extravascular lung water (pulmonary edema) has been demonstrated in humans with cor pulmonale, a condition characterized by systemic venous hypertension (SVH), rather than the pulmonary venous hypertension (PVH) seen in classic cardiogenic pulmonary edema due to left heart failure. 1 The latter may additionally show systemic venous hypertension recognized by the clinician as distended neck veins, hepatic congestion and edema of the extremities. Various forms of noncardiogenic pulmonary edema also are accompanied by elevation of central venous pressure (CVP) which is independent of the level of pulmonary venous pressure.2 ' 3 It has been postulated that the lung fluid accumulation seen in cor pulmonale is a conse-