Pulmonary artery infusion of prostacyclin increases lobar bronchial blood flow

Intrapulmonary systemic to pulmonary bronchial blood flow [Qbr (s-p)] decreases with administration of cyclooxygenase inhibitors. This effect may be due to a decrease in the production of vasodilating prostaglandins and reflect either a decrease in the total intrapulmonary bronchial blood flow (Qbr), or a redistribution of the intrapulmonary systemic venous return. In nine open chested dogs the left lower lobe (LLL) was isolated and perfused in situ. Blood flow to the extrapulmonary airways (Qep), and Qbr were measured by the reference flow technique. Qbr (s-p) was measured as the overflow from the closed LLL perfusion circuit. After ibuprofen, PG-I2 was infused into the LLL PA and the Qbr (s-p) was continuously monitored. Qbr, and Qep were measured before and after ibuprofen, and during and after the PG-I2 infusion. The upstream pressure for Qbr (s-p) was estimated with and without PG-I2 infusion. After ibuprofen the Qep, Qbr, and Qbr (s-p) fell to 45, 22, and 17%, respectively, of the pre-ibuprofen values (P less than 0.05). PG-I2 increased the Qbr (s-p) and Qbr (P less than 0.05), while Qep was unchanged. During all experimental conditions the simultaneous measurements of Qbr and Qbr (s-p) were not different from each other (P less than 0.001). The upstream pressure for Qbr (s-p) increased from 30 to 50 cm H2O (P less than 0.05). Intralobar bronchial blood flow is drained almost entirely through the pulmonary circulation, and PG-I2 in the LLL pulmonary circulation increases systemic blood flow to the LLL, probably acting at the level of a systemic arteriole.