Pulmonary complications are a major cause of death in patients in various forms of shock. The exact causes of the pulmonary complications are unknown. This study evaluates the functional characteristics of intralobar pulmonary arteries (IPA) and veins (IPV) obtained from swine subjected to splanchnic arterial occlusion (SAO) shock ans subsequent cardiovascular collapse and sham-shocked swine subjected to surgery but no occlusion. The contractile response of pulmonary arteries to norepinephrine (NE) and serotonin (5-HT) were depressed when obtained from pigs subjected to SAO shock. The depression in the sensitivity to 5-HT and maximal tension development to 5-HT and NE was selective, since the responses to potassium ion were not depressed. IPA obtained from swine with SAO shock were more sensitive to the relaxant actions of arachidonic acid, a precursor for bisenoic prostaglandins, than were IPA from sham-shocked swine. This was not observed when prostaglandins were used as agonists. This suggests that synthesis of prostaglandin differs in the pulmonary vasculature of sham-shocked and SAO-shocked animals. IPV obtained from swine in SAO shock were less sensitive to 5-HT and NE but more sensitive to arachidonic acid and 9 alpha, 11 alpha-epoxymethano-PGH2, a thromboxane like compound. IPV obtained from swine in SAO shock converted more arachidonic acid into a substance with the chromatographic mobility of thromboxane B2. The data suggest that alterations in the prostaglandin system within the pulmonary artery and vein may contribute to the pulmonary complications of SAO shock. The alterations appear to include an enhanced synthesis of prostacyclin as well as thromboxane-like substance. Because the veins were more sensitive than the arteries to 9 alpha, 11 alpha-epoxymethano-PGH2, thromboxanes or endoperoxides may elevate venous tone and contribute to the pulmonary edema associated with shock states.