Studies on the mechanism of the DEC reaction in dogs infected with Dirofilaria immitis

Studies have been undertaken to investigate a number of potential mediators of canine hepatic vein constriction, the key event in the DEC shock reaction in dogs infected with Dirofilaria immitis. Using an isolated canine hepatic vein preparation it has been shown that α-adrenergic, H1 histaminic and D tryptaminergic receptors are present. There is also evidence that M tryptaminergic receptors are located in this tissue. Bradykinin does not contract the isolated hepatic vein, while DEC in high concentrations causes a dose-dependent contraction which is not mediated through its known ability to release noradrenaline. In vivo experiments using pharmacological antagonists have confirmed that histamine, 5-hydroxytryptamine, noradrenaline and adrenaline are not involved in this reaction. The reaction was not blocked by the endorphin antagonists naloxone and meptazinol. Dexamethasone, but not indomethacin however did block the reaction. Both anti-inflammatory agents act on biosynthetic pathways from arachadonic acid leading to the formation of leukotrienes and prostaglandins, respectively. However, since the dog is insensitive to leukotrienes it seems unlikely that these autocoids mediate the reaction. Therefore, it is postulated that the reaction results from the release, by DEC, of substances from microfilariae which are able to contract the hepatic veins either directly or indirectly and so induce hepatic venous congestion and hypovolaemic shock.