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Lignocaine is used during intrapartum and postpartum period but there are conflicting reports regarding the effect of lignocaine on uterine contractility. Therefore, this study was undertaken to delineate the effect of lignocaine on uterine contractility and the underlying mechanisms.The in vitro contractions were recorded from the uterine segments obtained from adult rats (in estrous phase) and also from human myometrial tissue. Effect of lignocaine on spontaneous uterine contractions was recorded in the absence or presence of antagonists. Effect of sodium nitroprusside (SNP, NO donor) on uterine contractility was assessed. The NO2− was assayed (indicator of NO activity) from the supernatant after exposing the myometrial tissue to lignocaine in the absence or the presence of L-NAME or hemoglobin.Lignocaine (100 μM) increased the amplitude of uterine contractions by 75% with no alterations in frequency. Similar magnitude of increase was seen with human myometrial tissue also. The spontaneous activities were absent in Ca2+-free or in nifedipine (10 μM) containing medium. Heparin (IP3 blocker, 10 IU/ml), but not the indomethacin (10 μM) blocked the lignocaine-induced augmentation. L-NAME (NOS inhibitor, 10 μM) or methylene blue (guanylyl cyclase inhibitor, 100 μM) partially blocked the lignocaine-induced augmentation. SNP (30 μM) increased the amplitude of spontaneous uterine contractions. Lignocaine increased the NO2− content (indicator of NO activity) of uterine tissue and the increase was blocked by L-NAME or hemoglobin.Present observations indicate that lignocaine augments the amplitude of uterine contractions via Ca2+-dependent mechanisms involving NO-G cyclase-dependent mechanisms.Lignocaine augmented force of uterine contractility via Ca2+ mediated mechanismsInhibitors of NOS, G-cyclase or IP3 blocked lignocaine-induced augmentation.NO donor increased the force of uterine contractions similar to lignocaine.Lignocaine increased the NO content of uterine tissue and was blocked by NO antagonists.Lignocaine-induced response is mediated via NO-G-cyclase mediated mechanisms.