Pulmonary veins of rats have regular thin bands of constriction (sphincters) that deepen when the animals are given a blow to the head that is sufficient to cause pulmonary edema. Pulmonary edema caused by a stimulus to the brain is attenuated by alpha-adrenergic blockade. This study tested the hypothesis that alpha-adrenergic antagonism decreases this contraction in pulmonary veins. Male and female Sprague-Dawley rats were given prazosin, an alpha 1-specific antagonist, phentolamine, a combined alpha 1- and alpha 2-antagonist, or saline 10 min before their lungs were cast and they were given a blow on the head. The casts were fractured, causing the veins to break at the site of the constriction. Depth of contraction expressed as a percentage was 1 minus the ratio of the inner (constricted) and outer (total) diameters of the vein at the fracture. Resin that escaped the vascular space to cast alveoli and lymphatics was also measured. The average contraction of the veins at the site of the sphincters was 7.9 +/- 1.1% in the saline group, 5.4 +/- 0.7% in the phentolamine group, and 4.8 +/- 0.7% in the prazosin group (p < 0.05), although about a third of the constrictions were less than 2% in all groups. Arteries had no contraction. Contraction was greater in heavier and male animals, which were variables that interacted with the agent the animals were given in a multivariate analysis. Contrary to the hypothesis, lymphatic casts were greater in the animals receiving alpha-blockers (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)