Fadiga neuromuscular induzida por d-Tubocuranina, Hexametônio e Neostigmina em preparações nervo frênico-diafragma isolado de ratos diabéticos

Abstract

The acetylcholine released from motor nerve terminal (MNT) can regulate its own output (MNT automodulation) acting on nicotinic (positive feed back automodulation) or muscarinic (negative feedback automodulation) presynaptic receptors. On the other hand, diabetic neuropathy, a disorder of peripheral nerves, is one of the most common complication of diabetes mellitus that produces serious alterations on motor nerve terminal without interfering in the velocity and integrity of neuro-muscular transmission. Pharmacological studies have shown that diabetic animals are less sensitive to some neuromuscular blockades such as d-tubocurarine, galamine, pancuronium or decamethonium than normal ones. Results suggest that change in MNT automodulation may counterbalance neuronial deficiencies induced by diabetes. The present study with phrenic nerve-diaphragm preparations from normal and diabetic animals was conducted to verify whether differences in neuro-muscular fade induced by d-tubocurarine, hexametonium or neostimine exist. Results showed that there were no differences in neuro-muscular fade induced by neostigmine, hexametonium or d-tubocurarine. However, the recovery of tetanic fade induced by d-tubocurarine was faster in preparations obtained from diabetic rats. Difference might be explained by decrease in affinity of d-tubocurarine for presynaptic nicotinic receptors.