Continuous stimulation of transected distal nerves fails to prolong action potential propagation.

Department of Orthopaedic Surgery, SUNY at Downstate, Brooklyn, New York 11203, USA.
Clinical Orthopaedics and Related Research (Impact Factor: 2.88). 07/2006; 447:209-13. DOI: 10.1097/01.blo.0000203481.11797.0f
Source: PubMed

ABSTRACT Wallerian degeneration of the distal portion of a cut nerve is considered irreversible. A possible reason for degeneration is lack of axon stimulation in the distal, cut nerves. We hypothesized greater rates of stimulation of distal nerve stumps would prolong time to action potential propagation failure, and uncut nerves would not be damaged by implanted nerve stimulators. We also hypothesized that action potentials measured from the body of the sciatic nerve would show similar response as motor-evoked potentials measured in the muscles innervated by branches of the sciatic nerve. We implanted a nerve stimulator onto distal cut sciatic nerves of rats and recorded motor-evoked potentials. Three groups were stimulated at 1 Hz (once per second), 0.1 Hz (once per 10 seconds), and 0.01 Hz (once per 100 seconds) respectively. Motor-evoked potentials progressively declined after nerve transection, failing faster at 1 Hz (26.8 hours +/- 108 minutes) and 0.1 Hz (22 hours +/- 66 minutes) compared with stimulation at 0.01 Hz (36.75 hours +/- 83 minutes). Intact axons were not damaged by implanted nerve stimulators. Action potentials recorded directly from nerves were equivalent to motor- evoked potentials. Failure of motor-evoked potential transmission in a transected nerve is accelerated by a greater rate of continuous stimulation of the distal stump.

  • [Show abstract] [Hide abstract]
    ABSTRACT: The oculomotor nerve can regenerate anatomically and histologically after injury; however, the degree of functional recovery of extraocular muscles and the pupil sphincter muscle was not satisfactory. Electrostimulation was one potential intervention that was increasingly being studied for use in nerve injury settings. However, the effect of electrostimulation on regeneration of the injured oculomotor nerve was still obscure. In this study, we studied the effects of electrostimulation on neural regeneration in terms of neurofunction, myoelectrophysiology, neuroanatomy, and neurohistology after oculomotor nerve injury and found that electrostimulation on the injured oculomotor nerve enhanced the speed and final level of its functional and electrophysiological recovery, promoted neural regeneration, and enhanced the selectivity and specificity of reinnervation of the regenerated neuron, the conformity among the electrophysiological and functional recovery of extraocular muscles, and neural regeneration, and that the function of extraocular muscles recovered slower than electrophysiology. Thus, we speculated that electrostimulation on the injured oculomotor nerve produced a marked effect on all phases of neural regeneration including neuronal survival, sprout formation, axonal elongation, target reconnection, and synaptogenesis. We think that neural electrostimulation can be used in oculomotor nerve injury.
    Journal of Molecular Neuroscience 07/2014; · 2.76 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The sympathetic and parasympathetic divisions of the autonomic nervous system modulate cardiac rhythm and the probability of arrhythmia occurrence. Both increased sympathetic drive and hypoxia increase the likelihood for ventricular fibrillation (VF). Vagus nerve stimulation (VNS) can protect from fatal arrhythmias via cholinergic and nitrergic action. We sought to determine boundary conditions for VF and defibrillation by autonomic manipulations accompanied or not by hypoxic changes in urethane-anesthetized rats. VF was induced with (1) vagotomy, (2) systemic high-dose (>15 mg/kg) isoproterenol, and (3) hypoxemia. When VNS (50 Hz) produced cardiac standstill, it converted every VF episode (59/59). A nitric oxide synthase inhibitor did not reduce VNS efficacy (13/14 episodes converted), but addition of atropine reduced VNS efficacy (11/27 episodes converted). VF can be induced by autonomic derangements only under constrained conditions, including sympathetic over-activation, reduced parasympathetic input, and hypoxemia. VNS can provide an alternative method to defibrillate via its cholinergic action.
    The Journal of Physiological Sciences 08/2012; 62(6). · 1.25 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cardiac autonomic, conduction, and structural changes may occur in epilepsy and may contribute to sudden unexpected death in epilepsy (SUDEP), e.g. by increasing the risk for ventricular fibrillation (VF). In a model of chronic seizures in rats, we sought to study (1) cardiac and autonomic derangements that accompany the epileptic state, (2) whether chronically seizing rats experienced more significant cardiac effects after severe acute seizures, and (3) the susceptibility of chronically seizing rats to VF arising from autonomic and hypoxemic changes, which commonly occur during seizures. Sprague-Dawely rats were injected with saline or kainic acid to induce chronic seizures. At 2-3 months or 7-11 months after injection, these rats were studied with both 12-lead electrocardiography (to assess heart rate variability and QT dispersion) and echocardiography under ketamine/xylazine or urethane anesthesia. Hearts were subsequently excised, weighed, and examined histologically. Epileptic rats exhibited decreased vagal tone, increased QT dispersion, and eccentric cardiac hypertrophy without significant cardiac fibrosis, especially at 7-11 months post-injection. Of these three findings, vagal tone was inversely correlated with heart weights. Epileptic rats exhibited diminished systolic function compared to controls after severe acute seizures. However, animals with long-standing chronic seizures were less susceptible to autonomic/hypoxemia-driven VF, and their susceptibility inversely correlated with mean left ventricular wall thickness on histology. On the basis of this model, we conclude that cardiac changes accompany epilepsy and these can lead to significant seizure-associated cardiac performance decreases, but these cardiac changes actually lower the probability of VF.
    Epilepsy research 11/2013; · 2.48 Impact Factor