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

Abstract

Objective - To test the effect of heartworm infection on agonist- induced constriction of canine pulmonary artery and vein in vitro. Procedure - Cumulative concentration-response relations to norepinephrine, serotonin, histamine, prostaglandin F2α, 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. Animals - Noninfected control and heartworm-infected dogs. Results - There was no difference in constriction response to norepinephrine, serotonin, prostaglandin F2α, 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. Conclusion - 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 or decreases in the number of receptors expressed. Clinical Relevance - Mast cells and histamine may be important factors n altered endothelium-mediated responses associated with heartworm disease.