Pulmonary vasoconstriction during lidocaine administration are modulated by endothelium-derived relaxing factor.

We examined the role of endothelium-derived relaxing factor (EDRF) in lidocaine-induced pulmonary vasoconstriction in experiments using the nitric oxide synthase inhibitor NG-nitro-L-arginine (L-NNA) and EDRF precursor L-arginine in a canine cross-circulation model. The left lower lobe of one dog lung was perfused with venous blood from another dog at a constant rate of flow. Pretreatment of ibuprofen was performed to exclude the effects of vasoactive prostanoids. L-NNA significantly inhibited acetylcholine- and bradykinin-induced pulmonary vasodilation without affecting the vasodilatory responses to isoproterenol in pulmonary vessels preconstricted with thromboxane analogue U46619 or prostaglandin F2 alpha. Pulmonary vasoconstriction by 40 micrograms.ml-1 lidocaine infusion after pretreatment with L-NNA was significantly greater than that before pretreatment with L-NNA, and was reversed to the level present without L-NNA treatment by additional administration of L-arginine. We conclude that lidocaine-induced pulmonary vasoconstriction is modulated by the EDRF/NO pathway in dog lung.