Dirofilaria immitis: heartworm products contract rat trachea in vitro.

Subtle decreases in racing performance have been noted in asymptomatic greyhounds with heartworm burdens insufficient to obstruct pulmonary outflow, suggesting that alternative mechanisms may be involved in the pathogenesis of canine heartworm disease. Endothelium-dependent relaxation is depressed in the in vivo femoral artery of heartworm-infected dogs, in the in vitro pulmonary artery from heartworm-infected dogs, and in the in vitro rat aorta exposed to heartworms, heartworm-conditioned medium, and serum from heartworm-infected dogs. These findings suggest that circulating filarial factors may play a role in the pathogenesis of heartworm infection. We examined the effect of Dirofilaria immitis, the canine heartworm, on acetylcholine-induced contraction of rat tracheal rings. In epithelium-intact rings, both heartworms and heartworm-conditioned medium increased acetylcholine-induced contraction. Pretreatment of the parasites with aspirin prevented the filarial-induced increase in acetylcholine-induced contraction, suggesting that parasite cyclooxygenase products are responsible for the effect. In addition, heartworms caused contraction in both epithelium-intact and denuded rings and this effect was markedly decreased by pretreatment of the worms with aspirin. Filarial cyclooxygenase metabolites may cause airway hyperreactivity and parasite-derived factors could play a role in the subtle changes in exercise performance seen in asymptomatic greyhounds with low worm burdens. Comparable mechanisms may be operating in other filarial diseases, including those that affect humans in tropical countries.