mivacurium and Disease-Models--Animal

Recurrent laryngeal nerve palsy is a serious complication of endocrine surgery to the neck. Permanent lesions are still occurring in about one in a hundred, despite standardized surgical approach to the nerve and the availability of recurrent laryngeal nerve monitoring. Intraoperative recurrent laryngeal nerve monitoring is based on the visual or acoustic registration of evoked electromyography of the laryngeal muscles. Primarily, it proves conductivity of the stimulated nerve segment towards the muscle, so that stimulation distal of the lesion should show persistent electromyographic response.. In a porcine model, an iatrogenic nerve lesion of the recurrent laryngeal nerve was set. Subsequently, the proximal and distal dissected nerve portion was stimulated and the evoked electromyographic response of the laryngeal muscles was recorded by needle and laryngeal surface electrodes.. As expected, no signal was obtained from the proximal segment. Meanwhile, the distal segment showed unchanged amplitude of the electrophysiological response for the observation period of more than 1 h.. This result demonstrated a remarkable pitfall for the neuromuscular monitoring at the recurrent laryngeal nerve: In the human surgical setting, this might have resulted in the false assumption of an anatomical intact nerve. The persistence of distal electromyographic conduction strengthens the proposal to stimulate the vagal nerve as the proximal portion of the nerve as a part of a systematic protocol.

Topics: Animals; Bias; Disease Models, Animal; Electromyography; Humans; Iatrogenic Disease; Intraoperative Complications; Isoquinolines; Male; Mivacurium; Monitoring, Intraoperative; Neuromuscular Nondepolarizing Agents; Recurrent Laryngeal Nerve; Recurrent Laryngeal Nerve Injuries; Swine; Thyroid Diseases; Time Factors; Vagus Nerve; Vocal Cord Paralysis

The electrophysiologic actions of the competitive neuromuscular blocker mivacurium (0.05-0.8 mg/kg IV; N = 10) and atropine sulfate [0.01-0.16 mg/Kg intravenously (IV), N = 6] were determined under control conditions, during right vagus nerve stimulation, and during anterior right ganglionated plexus stimulation. Both drugs suppressed shortening of right atrial monophasic action potential (MAP) duration, right atrial refractoriness, and right superior pulmonary vein sleeve refractoriness produced by vagus nerve or ganglionated plexus stimulation and suppressed the induction of atrial fibrillation. Suppression of atrial fibrillation by atropine was accompanied by improved sinus and atrioventricular (AV) nodal function, increasing the ventricular heart rate observed during sinus rhythm and atrial fibrillation and eliminating the depressant actions of vagus nerve stimulation on sinoatrial (SA) and AV nodal function. Unlike atropine, mivacurium selectively antagonized the effects of vagus nerve and ganglionated plexus stimulation on atrial and pulmonary vein sleeve myocardium (shortening of action potential duration/refractoriness and increased atrial vulnerability) without altering sinus or AV nodal function under control conditions or during vagus nerve stimulation. The selective inhibition of parasympathetic nervous system effects in atrium versus sinus and AV nodes by mivacurium may represent a selective mechanism for the suppression of atrial fibrillation without altering SA and AV nodal function.

Topics: Action Potentials; Animals; Atrial Fibrillation; Atrioventricular Node; Atropine; Disease Models, Animal; Dogs; Dose-Response Relationship, Drug; Electrophysiology; Isoquinolines; Male; Mivacurium; Neuromuscular Nondepolarizing Agents; Parasympatholytics; Sinoatrial Node; Vagus Nerve

Neuromuscular blocking effects according to the severity of liver dysfunction have not been evaluated. We assessed the neuromuscular effects of mivacurium in carbon tetrachloride (CCl4)-treated rabbits with toxic hepatitis in vivo.. We compared the dose-response relationships and the neuromuscular blocking effects of mivacurium in 66 rabbits randomly treated with 0.3 mL kg(-1) of corn oil, 0.3 mL kg(-1) of CCl4 or 0.6 mL kg(-1) of CCl4 for 11 weeks, respectively. Train-of-four stimuli were applied every 10 s to the common peroneal nerve and the force of contraction of the tibialis anterior muscle was measured.. Severe hepatitis was associated with a rightward shift of the mivacurium dose-response curves, but mild hepatitis had no effect. The calculated ED50 values for the control, mild and severe hepatitis were 17.1+/-2.6, 18.2+/-2.7 and 31.8+/-3.2 microg kg(-1), respectively. Rabbits with severe hepatitis had a significantly prolonged recovery time from neuromuscular blockade compared with other rabbits. Cholinesterase activity had a negative correlation with recovery indices of mivacurium even in severe hepatic injury. Severe hepatitis induced a prolongation of action duration of repeated doses, but maintained the constant intervals.. The dose-response and the time course of neuromuscular blockade of mivacurium differ in mild hepatitis compared with severe hepatitis, but required no adjustments of different doses for repeated injection after the desired depth of neuromuscular block, and had a negative correlation with the activity of plasma cholinesterase in both hepatic injuries.

Topics: Animals; Biomarkers; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Cholinesterases; Disease Models, Animal; Dose-Response Relationship, Drug; Isoquinolines; Liver Function Tests; Male; Mivacurium; Muscle Relaxation; Neuromuscular Nondepolarizing Agents; Rabbits; Random Allocation; Time Factors