Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Muscle Denervation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 397 records · Page 22Linked to original sources
PubMedDate not supplied

Progressive latissimus dorsi muscle denervation for free-flap dynamic cardiomyoplasty.

BACKGROUND: The creation of free muscle grafts for surgical myoplasty is limited by the dependence of muscle on its original nerve supply. The aim of this study was to develop a model of gradual denervation of a large skeletal muscle (latissimus dorsi) and evaluate the possibility that atrophic degeneration and loss of function would be reduced using progressive nerve compression instead of surgical division of the nerve. The effects of chronic stimulation prior to, and after, denervation were also evaluated. METHODS: Electrodes connected to a myostimulator were implanted on 24 latissimus dorsi muscles of 12 goats. Denervation of these muscles was achieved either by sectioning of the nerve by progressive compression using ameroid rings placed around the nerve. Electrostimulation of the muscle started either 5 weeks before (prestimulation), or immediately after the denervation. RESULTS: The model of gradual nerve compression was successfully created and did have less atrophy and loss of function at mid-term when compared with nerve division. Chronic electrostimulation of the muscle after nerve division had a beneficial effect on function and on the atrophic process. Chronic electrostimulation in our model of gradual nerve compression did not mirror these beneficial results. Detrimental results were observed in groups in which chronic electrostimulation was applied prior to nerve division or constriction.

Animals↗
PubMed1987

Is there any difference between actins from intact and denervated muscles?

Various techniques have been used (UV absorbance and fluorescence spectroscopy, polarised UV fluorescence microscopy, viscosimetry, electrophoresis and isoelectric focusing, superprecipitation, etc.) As suggested by several parameters, denervation interferes with the structure of actin by producing local conformation changes in the region of aromatic residues near the sites responsible for actin-actin and actin-myosin interactions.

Actins↗
PubMed2001

Investigation of skeletal muscle denervation and reinnervation using magnetic resonance spectroscopy.

OBJECTIVE: To determine changes in skeletal muscle metabolism after nerve transection and repair and to correlate metabolic changes with functional recovery. STUDY DESIGN AND SETTING: Male Wistar rats were divided into 6 experimental groups plus a control group. The posterior tibial nerve was transected and reapproximated. At varying times after surgery (1, 2, 4, 6, or 8 weeks) animals were sacrificed, the gastrocnemius muscle was harvested, and proton nuclear magnetic resonance (NMR) spectroscopy was performed. Functional recovery was measured using the sciatic function index. RESULTS: Animals undergoing nerve repair all showed functional recovery whereas the nonrepaired nerve group did not. Concentration of glucose and lactate increased after denervation and then returned toward normal. Choline concentration decreased and then returned toward normal. In animals not undergoing nerve repair, the metabolic abnormalities persisted and showed no sign of recovery over the 8-week observation period. CONCLUSIONS: 1H NMR spectroscopy is a potentially useful tool to study changes in skeletal muscle metabolism after motor nerve injury. SIGNIFICANCE: NMR spectroscopy is rapidly developing into a clinically useful tool. High-field magnets have improved resolution and data acquisition. Basic experiments, such as those described here, will help guide the use of NMR spectroscopy in clinical medicine and will also lead to a better understanding of basic mechanisms of nerve injury and repair.

Action Potentials↗
PubMed1975

Contractile inactivation in frog single denervated muscle fibers.

After preliminary conditioning depolarizations, single muscle fibers of the frog were tested for ability to contract in response to depolarization by 100 mM K+ Ringer solution. Denervated fibers (6-42 days) lose their ability to produce a 100 mM K+ contracture more rapidly than do control fibers. This decrease in 100 mM K+ contracture size (inactivation) is dependent on length of exposure to and magnitude of the conditioning depolarization and on the calcium concentration in the external medium. At 0.4 mM Ca++, the inactivation is 3 times faster than at 1.5 mM Ca++. The rate of contracture loss is not correlated with fiber diameter or the number of days after failure of neuromuscular transmission, and the preliminary conditioning depolarizations do not affect the rate of terminal relaxation from the 100 mM K+ contractures.

Animals↗
PubMed1997

The effect of duration of muscle denervation on functional recovery in the rat model.

The effect of long-term denervation on neuromuscular recovery was studied in a rat hind limb model. The posterior tibial nerve was transected and repaired immediately or after denervation periods of 2 weeks, or 1, 3, 6, 9, or 12 months. Six months following reconstruction excellent axonal regeneration was seen across all nerve repairs irrespective of periods of denervation. However, there was a precipitous and profound decrease in the recovery of both muscle mass and integrated motor function if the reconstruction was delayed for longer than 1 month. Rather than a progressive change proportional to the length of the denervation period, significant, more discrete changes occurred sometime after 1 month of denervation that precluded a full recovery of muscle mass. Integrated motor function quantified using walking track analysis was impaired even after immediate nerve repair.

Animals↗
PubMed1976

The angio-architecture of normal, hypertrophic and denervated muscle. A study in the rat, using micro-angiography and the scanning electron microscope.

The angio-architecture of normal, hypertrophic and denervated rat muscles was studied by micro-angiography and by scanning electron microscopy of vascular casts made of methylmethacrylate. In hypertrophy, there was a slightly coarse-meshed irregular capillary network with some loss of normal parallelism, an increased calibre and a slight spiralization of all vessels. Probably all these changes, except the slight spiralization, increase the circulation. In denervation atrophy, the vascular pattern was much more irregular, with much more marked spiralization and loss of parallelism and narrowed capillaries. The changes probably contribute to the impairment of the circulation.

Animals↗
PubMed2004

Nitric oxide involvement in reperfusion injury of denervated muscle.

PURPOSE: To investigate whether inhibition of inducible nitric oxide synthase (iNOS) improves microcirculation in denervated and reperfused skeletal muscle. METHODS: The cremaster muscles of 52 rats received iNOS inhibitor 1400W (3 mg/kg) or phosphate buffered saline (PBS) and underwent either 3 hours of ischemia and 1.5 hours of reperfusion or a sham operation. During reperfusion the vessel diameters were measured by using intravital videomicroscopy and overall muscle blood flow was measured with laser Doppler flowmetry. The expression of NOS messenger RNA (mRNA) and protein was determined by using real-time reverse-transcription polymerase chain reaction and Western blot, respectively. RESULTS: 1400W treatment significantly increased the mean blood flow of the reperfused muscle compared with controls, and this was associated with significantly less vasospasm in 10 to 20 microm, 21 to 40 microm, and 41 to 70 microm arterioles. The expression of iNOS mRNA and protein in controls increased 23-fold and 6-fold from normal, respectively, but was reduced to only a 2-fold increase in the 1400W-treated muscles. The ischemia/reperfusion (I/R)-induced decrease of endothelial NOS (eNOS) and neuronal NOS (nNOS) expression in controls was not significantly changed after 1400W treatment. CONCLUSIONS: Our data support a nitric oxide-mediated mechanism in reperfusion injury and show the importance of inhibition of iNOS in reducing reperfusion injury in denervated skeletal muscle. Our results suggest potential benefits via inhibition of iNOS to improve clinical outcomes not only for hand surgeons who work in the microsurgery field, but also for other physicians whose work involves ischemia/reperfusion injury.

Amidines↗
PubMed1951

The behavior of residual axons in partially denervated muscles of the monkey.

Leg muscles of the monkey have been studied following partial denervation produced by surgical elimination of from 25 to 90 per cent of the axons entering the sciatic nerve from the lumbosacral plexus. The investigation included observations on function, rate and degree of muscle atrophy, and neurohistological appearance of the affected muscles. In most of the cases, from 83 to 90 per cent of the residual nerve fibers in the peroneal and tibial nerves were destroyed and a severe paresis of the leg muscles was produced. No functional improvement was noted up to 160 days after operation, and the affected muscles became markedly atrophic. Histological examination of these muscles failed to reveal more than sporadic collateral regeneration of the residual axons. In two cases 50 and 75 per cent of the peroneal and tibial nerve fibers remained intact 63 and 200 days, respectively, after operation. The legs operated upon in these cases functioned almost normally and all muscles weighed within 11 per cent of those of the contralateral, normal leg. Histological study and counts of end-plate: nerve fiber ratios showed that many residual axons had regenerated collateral branches which entered denervated end-plates. Collateral regeneration was incomplete, however, and many end-plates remained without innervation. These results indicate that residual axons in paretic muscles of a primate do not regenerate collaterally as readily as do those of other previously studied mammals.

Animals↗
PubMed1999

Computer simulation of field distribution and excitation of denervated muscle fibers caused by surface electrodes.

In the course of this study, 2 submodels have been developed and combined, the 2-D finite element modeling of the electrical potential distribution in the human thigh and a Hodgkin and Huxley (HH) type model to calculate fiber excitation and action potential propagation. To determine the excitation of the target muscle fiber with the help of the activating function, the fiber's orientation within the muscle has to be known. The electric field along the fiber has to be calculated as a function of the applied electric current and the potential at the electrodes, respectively. The excitement of the muscle fibers varies across a wide range depending on the active and passive membrane parameters and the intracellular and extracellular mediums. Persisting denervation leads to a decay of muscle cells, and a partial substitution by fibroblasts occurs. The electrical activation of these tissues is more difficult, and biphasic stimulation pulses up to 200 ms in duration and 60-100 V in amplitude are needed to cause a contraction of the denervated muscle. An example shows the field distribution and the simulated activity in one representative muscle fiber of a well trained m. rectus femoris.

Action Potentials↗
PubMed1996

[Magnetic resonance tomography and histopathologic findings after muscle denervation. A comparative animal experiment study during a two month follow-up].

Recently, MRI was described as a method in the diagnosis of changes of muscle after acute neurogenic muscle atrophy. This study was performed to compare MRI results with myopathological findings, to document the appearance of the MRI changes and to check the sensitivity of this method. We performed a segment resection of the suprascapular nerve resulting in a denervation of the supraspinatus and infraspinatus muscles on 18 Newzeeland white rabbits. MRI changes were followed and documented for two months in short periods of time. The results were compared with histological findings. In myopathology and MRI we found systematical changes: Apart from the reduction of the muscle diameter visual assessment revealed increased signal intensities on the 21st and 35th examination day after denervation. On the 2nd, 5th, 11th and 64th examination day signal intensities were normal. The changes were represented by calculated T2 times, too.

Animals↗
PubMed1991

Recovery of denervated muscle receptors following treatments to accelerate nerve regeneration.

Nerve regeneration promoters offer the possibility of enhancing recovery following nerve injury by increasing the numbers of regenerating axons and decreasing the period of tissue denervation. To date, recent studies have concentrated on evaluating the action of such promoters on the nerve itself and on the restoration of motor function. This study examines afferent regeneration by evaluating the recovery of muscle spindles and tendon organs after nerve injury and treatment with alpha-melanocyte stimulating hormone or nerve stimulation. Treatment was found to be effective in enhancing short-term recovery after nerve-crush injury in terms of increasing the rate of functional and morphological recovery. Following nerve section, there was an increase in the number of reinnervating axons compared with control values.

Animals↗
PubMed1999

Loss of distal axons and sensory Merkel cells and features indicative of muscle denervation in hindlimbs of P0-deficient mice.

Mice lacking the major Schwann cell myelin component P0 show a severe dysmyelination with pathological features reminiscent of the Déjérine-Sottas syndrome in humans. Previous morphological and electrophysiological studies on these mice did not only demonstrate a compromised myelination and myelin maintenance, but were suggestive of an impairment of axons as well. Here, we studied the axonal pathology in P0-deficient mice by quantitative electron microscopy. In addition, we investigated epidermal receptor end organs by immunocytochemistry and muscle pathology by histochemistry. In proximal sections of facial and femoral nerves, axon calibers were significantly reduced, whereas the number of myelin-competent axons was not diminished in 5- and 17-month-old P0-deficient mice. However, in distal branches of the femoral and sciatic nerve (digital nerves innervating the skin of the first toe) the numbers of myelin-competent axons were reduced by 70% in 6-month-old P0-deficient mice. Immunolabeling of foot pads revealed a corresponding loss of Merkel cells by 75%, suggesting that survival of these cells is dependent on the presence or maintenance of their innervating myelinated axons. In addition, quadriceps and gastrocnemius muscles showed pathological features indicative of denervation and axonal sprouting. These findings demonstrate that loss of an important myelin component can initiate degenerative mechanisms not only in the Schwann cell but also in the distal portions of myelinated axons, leading to the degeneration of specialized receptor end organs and impairment of muscle innervation.

Animals↗