Lidocaine‐induced hemodynamic effects are enhanced by the inhibition of endothelium‐derived relaxing factor in dogs

Background: Lidocaine has been shown to have direct vasoconstrictive effects at low concentrations. Since lidocaine inhibits endothelium‐dependent vasodilation in vitro , the vasoconstrictor effect of lidocaine may be due to inhibition of endothelium‐derived relaxing factor(EDRF/NO). Therefore, the current study was designed to determine the effects of N G ‐nitro‐L‐arginine (L‐NNA), a potent inhibitor of nitric oxide synthase, on systemic and pulmonary hemodynamics during lidocaine infusion. Methods: Systemic and pulmonary hemodynamic effects of lidocaine infusion, 1 mg kg ‐1 min ‐1 , for 10 min were measured in dogs anesthetized with 1% halothane in oxygen. Dogs were studied twice with an interval of 1 week in a cross‐over study, and were assigned to one of two groups that received saline or L‐NNA intravenously in group 1 (n=8), or L‐NNA or L‐NNA+L‐arginine which reverses the nitric oxide synthesis inhibitor effect of L‐NNA, intravenously in group 2 (n=8) prior to lidocaine infusion. The free serum concentration of and protein‐binding ratio for lidocaine were measured. Results: With saline pretreatment in group 1, lidocaine infusion significantly decreased cardiac index (CI) and significantly in‐ Conclusion: In contrast to in vitro study, vasoconstrictor effect of lidocaine is enhanced when a capacity for compensatory vasodilation including EDRF/NO pathway is exhausted in halo‐thane‐anesthetized dogs.