Denervated muscle fibres in hereditary mouse dystrophy.
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In order to explore the possibility of clinical application of laryngeal pacing as a treatment for unilateral vocal cord paralysis, we examined the reactivity of atrophic muscle to electrical stimulation in dogs whose recurrent laryngeal nerves were damaged by crushing, dissection followed by resuturing, or a 3-cm neurectomy. The threshold level to induce enough vocal cord adduction reached the maximum at 2 weeks after nerve injury, decreased with time, and never surpassed 7 V in each case. On the basis of results of these preliminary probings, laryngeal pacing was conducted on a dog 15 months after resection of the laryngeal nerve. Adduction of the paralyzed vocal cord for synchrony with the intact cord was achieved by 7 V of electrical stimulation of the thyroarytenoid muscle that was triggered by signals from the cricothyroid muscle.
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A systematic study of dystrophy-denervation in human muscle showed minimal morphometabolic differences between dystrophic and dystrophic-denervated muscle. The only certain conclusion is that denervation influences the rhythm of evolution of the dystrophy without impressing any of the few characteristics considered at present as peculiar to denervation.
The study was conducted to determine if daily electrical stimulation of denervated muscle, initiated the day following crush denervation and continued for 8 weeks (i.e., 5 weeks after presumptive reinnervation), would influence denervation-associated alterations in muscle size and in situ contractile properties of rat gastrocnemius. A stimulation protocol of brief, strong, isometric contractions was designed to maximize the beneficial effects as described by previous authors. By 8 weeks after crush, unstimulated muscles were still significantly lighter in wet weight, were tetanically weaker, and showed slower isometric contractile responses in situ than controls. Denervated muscles which had been stimulated daily were heavier and tetanically stronger (the latter not different from controls) than those in the nonstimulated group. Muscle weights from groups of animals killed at 2 or 4 weeks after nerve crush indicated the major benefit of stimulation occurred during this initial 4-week period. In situ fatigue properties were unaffected by denervation or stimulation. A protocol of electrical stimulation-evoked strong contractions, initiated soon after denervation and continued after reinnervation, was effective in attenuating the strength-related, but not speed-related, changes in neuromuscular function resulting from denervation. These latter changes are presumably the result of loss of "neurotrophic influence" and/or continuous low-tension muscle activity lost as a result of denervation.
The purpose of this study was to test the hypothesis that extrinsic mechanical factors, i.e., the dynamic shortening and lengthening imposed on a muscle during limb movements and the rhythmic compressions as surrounding muscles contract and relax, contribute to the initial muscle hyperemia during locomotion in conscious male Sprague-Dawley rats. Soleus and lateral head of gastrocnemius muscles were surgically denervated in one hindlimb several hours before exercise to remove 1) local metabolic vasodilator effects, 2) vasoconstrictor or vasodilatory influences mediated through sympathetic postganglionic fibers, and 3) intrinsic mechanical pumping. Blood flow was measured with radioactive microspheres during preexercise and at 30 s and 5 min of exercise in rats walking at 15 m/min or a motor-driven treadmill. Glycogen concentrations were also measured as an indicator of muscular activity to verify the denervation. Blood flows to control muscles in the normal limb were similar to previously reported values during preexercise and exercise. Denervation, however, decreased preexercise blood flow (69-88%) to muscle composed predominantly of oxidative fibers and increased flow (53%) to muscle composed predominantly of glycolytic fibers. During exercise, blood flow to denervated muscles either remained unchanged or decreased. These data suggest that extrinsic mechanical factors do not significantly contribute to the initial hyperemic response at the onset of low-intensity exercise in normal muscle.