[Influence of lidocaine on the neuromuscular block produced by rocuronium: study in rat phrenic-diaphragmatic nerve preparation.].

BACKGROUND AND OBJECTIVES The action mechanism of local anesthetics (LA) on neuromuscular junction motivated several studies. When administered at low doses, they do not interfere on neuromuscular transmission. But high doses may compromise neuromuscular transmission and increase the effects of neuromuscular blockers. The objective of this study was to evaluate lidocaine interaction with rocuronium on rat diaphragm through its influence on neuromuscular block degree. METHODS Rats, weighing between 250 and 300 g, were used. Preparation was set according to the technique described by Bulbring. Groups were formed (n = 5) according to the drug being studied: lidocaine - 20 microg.mL-1 (Group I); rocuronium - 4 microg.mL-1 (Group II), and rocuronium - 4 microg.mL-1 with lidocaine - 20 microg.mL-1 (Group III). The following items were assessed: 1) the extent of diaphragm muscle responses to indirect stimulation, both before and 60 minutes after adding lidocaine and a neuromuscular blocker; 2) membrane potentials (MP) and miniature end-plate potentials (MEPP); 3) the effectiveness of neostigmine, and 4) aminopyridine on neuromuscular blockage reversal. RESULTS When administered separately, lidocaine did not alter the extent of muscular responses. With the previous use of lidocaine, rocuronium neuromuscular blockage was 82.8% +/- 1.91%, with a significant difference (p = 0.0079) when compared to the group with isolated rocuronium (57.8% +/- 1.9%). Blockage was both partially and fully reverted by neostigmine and 4-aminopyridine, respectively. Lidocaine did not alter membrane potential and caused an initial increase on MEPP, followed by a blockage. CONCLUSIONS Lidocaine increases the neuromuscular blocking produced by rocuronium. MEPP modifications identify a presynaptic action. The complete antagonism of 4-aminopyridine indicates a presynaptic component. This idea is supported by the partial antagonism through neostigmine.