Transmission of mepivacaine hydrochloride (carbocaine) across the human placenta

Lidocaine administered at a continuous rate infusion does not impair left ventricular systolic and diastolic function of healthy rabbits sedated with midazolam.

Differential effects of four xylidine derivatives in the model of ischemia- and re-perfusion-induced arrhythmias in rats in vivo.

The potential mechanism of mepivacaine’s myocardial depressant effect observed in papillary muscle has not yet been investigated at cellular level. Therefore, we evaluated mepivacaine’s effects on Ca2+ transient in isolated adult mouse cardiomyocytes. Single ventricular myocytes were enzymatically isolated from wild-type C57Bl/6 mice and loaded with 10 μM fluorescent Ca2+ indicator Fluo-4-AM to record intracellular Ca2+ transients upon electrical stimulation. The mepivacaine effects at half-maximal inhibitory concentration (IC50) was determined on calibrated cardiomyocytes’ Ca2+ transients by non-parametric statistical analyses on biophysical parameters. Combination of mepivacaine with NCX blockers ORM-10103 or NiCl2 were used to test a possible mechanism to explain mepivacaine-induced Ca2+ transients’ reduction. A significant inhibition at mepivacaine’s IC50 (50 μM) on Ca2+ transients was measured in biophysical parameters such as peak (control: 528.6 ± 73.61 nM vs mepivacaine: 130.9 ± 15.63 nM; p < 0.05), peak area (control: 401.7 ± 63.09 nM*s vs mepivacaine: 72.14 ± 10.46 nM*s; p < 0.05), slope (control: 7699 ± 1110 nM/s vs mepivacaine: 1686 ± 226.6 nM/s; p < 0.05), time to peak (control: 107.9 ± 8.967 ms vs mepivacaine: 83.61 ± 7.650 ms; p < 0.05) and D50 (control: 457.1 ± 47.16 ms vs mepivacaine: 284.5 ± 22.71 ms; p < 0.05). Combination of mepivacaine with NCX blockers ORM-10103 or NiCl2 showed a significant increase in the baseline of [Ca2+] and arrhythmic activity upon electrical stimulation. At cellular level, mepivacaine blocks Na+ channels, enhancing the reverse mode activity of NCX, leading to a significant reduction of Ca2+ transients. These results suggest a new mechanism for the mepivacaine-reduction contractility effect.

/pdf/mepivacaine-reduces-calcium-transients-in-isolated-murine-3m3kpbtcyo.pdf

Mepivacaine reduces calcium transients in isolated murine ventricular cardiomyocytes.

With regard to the inhibition of contractility, dose-response curves of ryanodine and nickel were produced, and in these curves ID50 values were 10(-6) M and 2 x 10(-3) M, respectively. ID50 of bupivacaine was similar to ryanodine's and that of lidocaine was between ryanodine and nickel. On the post-rest potentiation (PRP) elicited after 2 s of rest following a train of stimulation at 3 Hz, ryanodine and bupivacaine had similar depressing effects, but lidocaine depressed it moderately and nickel showed no effect. These results suggest that bupivacaine could cause a direct inhibitory effect on sarcoplasmic reticulum (SR) function like ryanodine, but lidocaine could cause mainly a reduction in trans-sarcolemmal Ca influx and induce a slight inhibitory effect on SR function.

[The effect of local anesthetics on the isolated human right atrial appendages--Part 2: Bupivacaine is different from lidocaine concerning the mechanism of inhibition of contractility].

Background and objective: To compare the inotropic and lusitropic effect of lidocaine and mepivacaine on rat papillary muscle. Methods: Effects of lidocaine and mepivacaine (10 -8 -10 -3 M) were studied in rat left ventricular papillary muscles in vitro at a calcium concentration of 1 mmol, under low (isotonic) and high (isometric) loads. Results: Lidocaine induced a significant negative inotropic effect in isotonic and isometric conditions whereas mepivacaine did not. Mepivacaine only induced a negative inotropic effect when added as a bolus for the highest concentration and this effect was significantly more pronounced with lidocaine than with mepivacaine (active force at 10 -3 M: 63 ± 10 vs. 84 ± 10% of baseline, P < 0.05). Increasing calcium concentration resulted in a greater positive inotropic effect in the control (199 ± 11% of baseline) and mepivacaine groups (197 ± 22% of baseline) when compared to the lidocaine group (163 ± 19% of baseline, P < 0.05 vs. lidocaine and control groups), suggesting an impairment on intracellular Ca 2+ handling by lidocaine. A negative lusitropic effect under low load was observed only for mepivacaine and suggested an impairment of sarcoplasmic reticulum function. Lidocaine and mepivacaine did not modify postrest potentiation but significantly depressed the force-frequency relationship. Conclusions: The negative inotropic and lusitropic effects induced by lidocaine were more important than that of mepivacaine and may involve an impairment of intracellular Ca 2+ handling.

Comparison of the effects of mepivacaine and lidocaine on rat myocardium.

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Comparison of the effects of mepivacaine and lidocaine on rat myocardium.