The association of pulmonary edema with catecholamine excess was recognized more than a century ago by investigators who found that high-dose epinephrine reliably induced cardiopulmonary failure in various animal models of shock.2,3 Berk et al4 showed detrimental effects on pulmonary gas exchange after infusion of epinephrine in anesthetized dogs. We reported the acute deterioration of arterial oxygen tension and pulmonary gas exchange in rats within a minute of bolus epinephrine administration. Interestingly, this effect was attenuated or completely prevented by pretreatment with phentolamine.5 Although the mechanism continues to remain speculative, preliminary studies in our isolated murine lung model suggest that catecholamine-induced pulmonary edema and secondary hypoxemia result from the combination of increases in pulmonary capillary pressure and shear injury secondary to elevated cardiac output. The use of α blockade may help correct one factor of this pathophysiologic equation and, thereby, improve gas exchange. This putative explanation of our experimental observations should also apply to the clinical success of phentolamine in repairing severe neurogenic pulmonary edema.