Role of circulating blood components and thromboxane in anaphylactic vasoconstriction in isolated canine lungs.

We determined the roles of circulating blood components and chemical mediators in anaphylactic vasoconstriction and microvascular permeability during Ascaris suum antigen-induced anaphylaxis in isolated canine lungs. Either the right or left lower lobe served as the control lung, which was perfused with autologous blood, and the contralateral lobe from the same dog was examined for the effect of albumin Krebs-Henseleit solution (Krebs) or of blockers of various vasoconstrictors with blood perfusion. Pulmonary vasoconstriction occurred after injection of the antigen (15 mg) in both the blood- and Krebs-perfused lungs. However, the percent change of peak pulmonary vascular resistance in the Krebs-perfused lungs tended to be greater than that in the blood-perfused lungs (689.9 +/- 289.3 and 389.3 +/- 171.9%, respectively). This increased peak pulmonary vascular resistance was attenuated similarly by pretreatment with indomethacin (1.1 x 10(-4) M; cyclooxygenase inhibitor), AA-2414 (10(-5) M; thromboxane-receptor antagonist), or a combination of TCV-309 (10(-5) M; platelet-activating factor-receptor antagonist), diphenhydramine (1.7 x 10(-4) M, histamine H1-receptor antagonist), and indomethacin but not by pretreatment with TCV-309 or diphenhydramine alone. The filtration coefficient, an index of vascular permeability, did not change significantly at 15 or 60 min after the antigen in all groups. These findings suggest that anaphylactic vasoconstriction in the isolated canine lung is independent of circulating blood components. Thromboxane is the major mediator for the anaphylactic vasoconstriction. Anaphylaxis does not increase pulmonary vascular permeability in isolated canine lungs.