Abstract

In acute experiments on rats, we examined the effects of course systemic introduction of sodium gammahydroxybutyrate (NaGHB, 100 mg/kg, i.p., daily within 3 weeks) on consequences of compression of the right sciatic nerve, SN. In the control group, the nerve was compressed, but NaGHB was not injected. Electrical and force responses of the m. gastrocnemius+soleus (GS) and m. tibialis anterior (TA) evoked by stimulation of the n. tibialis comm. and n. peroneus comm., respectively, at the side of SN impairment and the opposite intact side were recorded. Compression of the SN induced in animals of the control group (with no injections of NaGHB) considerable increases in the values of the threshold and chronaxia of the stimulated nerve, decreases in the amplitude of EMG responses of the muscles, increases in the latencies of these reactions, and also decreases in the force responses developed at single and tetanic isometric contractions of the above muscles. At the side of SN compression, graphs of recovery of the second muscle response under conditions of paired stimulation of the nerves were shifted toward greater interstimulus intervals. Course introduction of NaGHB resulted in more than a twofold increase in the thresholds upon stimulation of the nerves; at the same time, the chronaxia values decreased. The amplitudes of EMG responses of the muscles after NaGHB injections became smaller than in the control, and the latencies of these responses increased. Under these conditions, curves of recovery of the second response at paired stimulation were shifted toward shorter interstimulus intervals. Introduction of NaGHB provided noticeable increases in the force responses of the tested muscles. Such changes were observed bilaterally, and the relative intensities of the corresponding modifications at the side of SN compression and the intact side were close to each other. Possible mechanisms of the effect of NaGHB on the state of the nerve/muscle apparatus of the limb after compression of a large nerve trunk resulting in the development of traumatic neuropathy are discussed.

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