Effect of heartworm infection on in vitro contractile responses of canine pulmonary artery and vein.

To test the effect of heartworm infection on agonist-induced constriction of canine pulmonary artery and vein in vitro. Cumulative concentration-response relations to norepinephrine, serotonin, histamine, prostaglandin F2 alpha, and the thromboxane A2 analog U-44069 were determined, using isolated rings of pulmonary artery and vein from control and heartworm-infected dogs. To determine the role of endothelial cells in histamine constriction, some rings were denuded of endothelial cells in both artery and vein. Noninfected control and heartworm-infected dogs. There was no difference in constriction response to norepinephrine, serotonin, prostaglandin F2 alpha, or U44069 of pulmonary artery or vein from control or heartworm-infected dogs. Histamine-induced constriction of pulmonary artery from heartworm-infected dogs was not different from control values, however, when endothelial cells were removed from control, but not heartworm-infected pulmonary artery, histamine-induced constriction was enhanced. Histamine-induced constriction of pulmonary vein from heartworm-infected dogs was significantly depressed, compared with that of control pulmonary vein. However, removal of endothelial cells in pulmonary vein from heartworm-infected, but not control dogs significantly increased constriction. Heartworm infection alters histamine-induced constriction responses of pulmonary artery and vein. These changes may reflect high circulating histamine concentrations in heartworm-infected dogs, compared with that in controls. Increased circulating histamine concentrations in vivo could bring about decreased sensitivity of histamine receptors o decreases in the number of receptors expressed. Mast cells and histamine may be important factors in altered endothelium-mediated responses associated with heartworm disease.