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PubMed1992

Delayed debulking of free muscle flaps for aesthetic contouring debulking of free muscle flaps.

Although denervated muscle and myocutaneous free flaps atrophy over a period of time, when used for surface coverage they may remain bulky, resulting in a less than optimal aesthetic result. With the availability of a number of donor sites, soft tissue defects can often be reconstructed with like tissue in a single stage. Even though the goal of all plastic surgeons is to achieve a good cosmetic result, special circumstances might dictate that need take precedence over form. We have had six cases where a bulky muscle was used to achieve well vascularised coverage. After wound closure had been successfully accomplished, a secondary debulking procedure was performed safely for a final acceptable aesthetic result.

Adolescent↗
PubMed1979

Desensitization of glutamate receptors on innervated and denervated locust muscle fibres.

Depolarizations to L-glutamate, applied locally by microinophoresis to the extrajunctional membrane of locust extensor tibiae muscle fibres and measured either in current clamp or voltage clamp, increased in amplitude for equivalent doses of glutamate following chronic denervation of the muscle. 2. A two-pulse method was used to examine recovery from desentization of junctional and extrajunctional receptors. A 'response ratio', i.e. the amplitude of response to the second (test) of a pair of glutamate pulses over to the pulses. The 'response ratio' for extrajunctional depolarizations of innervated fibres increased exponentially with pulse interval, with a time constant of 15.6 +/- 4.7 sec (n = 11). Recovery of extrajunctional receptor populations from desensitization was accelerated after denervation. The recovery kinetics for responses from fibres 6-22 days after denervation were generally described by two exponential terms, with time constants in the range 0.5-10 sec which were inversely related to the glutamate sensitivity of the extrajunctional membrane. For junctional receptors on both innervated and denervated fibres the recovery kinetics were described by a single exponential with a time constant of 0.2-1 sec. 3. The results suggest that the increased extrajunctional glutamate sensitivity which occurs after denervation results from the 'appearance' of glutamate receptors with properties similar to those found at the post-junctional membrane on locust muscle fibres.

Animals↗
PubMed1999

A regenerative change during muscle adaptation to denervation in rats.

The purpose of this study is to examine the cellular and molecular events coincident with muscle denervation, especially the regenerative changes seen following muscle denervation, the role of satellite cells in this process, and the possibility of apoptotic degeneration of myonuclei as a mechanism of myonuclei loss during muscle denervation atrophy. Myosin heavy chain (MHC) isoform expression during muscle denervation was examined using pyrophosphate acrylamide gel electrophoresis and immunohistochemistry. DNA fragmentation (apoptosis) in myonuclei of denervated fibers was investigated using agarose gel electrophoresis, the TUNEL technique and ELISA for cytoplasmic histone-associated DNA fragmentation. Immunohistochemistry for MyoD and BrdU was also performed. Following muscle denervation, embryonic MHC, which is not expressed in adult healthy muscles, was expressed in some denervated fibers as well as in small activated satellite cells; maximal expression was observed 2 to 3 weeks after denervation. Activation and proliferation of satellite cells were observed, while few typical regenerating fibers were identified. It is speculated that most activated satellite cells fused to the denervated maternal fibers in order to repair them instead of fusing to each other to form new fibers as a mechanism that compensates for the atrophic changes after denervation. Although DNA ladder formation was not observed with agarose gel electrophoresis, DNA fragmentation was detected by the TUNEL technique and ELISA, suggesting that apoptotic degeneration contributes to the loss of myonuclei associated with denervation atrophy.

Animals↗
PubMedDate not supplied

Mechanisms controlling axonal sprouting at the neuromuscular junction.

This review considers the relative roles of sprouting stimuli, perisynaptic Schwann cells and neuromuscular activity in axonal sprouting at the neuromuscular junction in partially denervated muscles. A number of sprouting stimuli, including insulin-like growth factor II, which are generated from inactive muscle fibers in partially denervated and paralyzed skeletal muscles, has been considered. There is also evidence that perisynaptic Schwann cells induce and guide axonal sprouting in adult partially denervated muscles. Excessive neuromuscular activity significantly reduces bridging of perisynaptic Schwann cell processes between innervated and denervated endplates and thereby inhibits axonal sprouting in partially denervated adult muscles. Elimination of neuromuscular activity is also detrimental to sprouting in these muscles, suggesting that calcium influx into the nerve is crucial for axonal sprouting. The role of neuromuscular activity in axonal sprouting will be considered critically in the context of the roles of sprouting stimuli and perisynaptic Schwann cells in the process of axonal sprouting.

Animals↗
PubMed1992

Localization of the Ca(2+)-dependent proteinases and their inhibitor in normal, fasted, and denervated rat skeletal muscle.

Immunofluorescence and immunogold localization studies show that the two Ca(2+)-dependent proteinases (mu-calpain for the micromolar Ca(2+)-requiring proteinase and m-calpain for the millimolar Ca(2+)-requiring proteinase) and their protein inhibitor (calpastatin) are located exclusively intracellularly in normal rat soleus muscle. Quantitative immunogold studies indicate that binding of antibodies to both calpains and to calpastatin is approximately two times greater at the Z-disk of myofibrils than it is at the I-band or A-band regions. Mitochondria and nuclei in muscle cells contain both calpains and calpastatin at concentrations approximately one-tenth and one-fifth, respectively, of the concentration at the Z-disk, as estimated by antibody binding. Very little calpain or calpastatin was seen in the cytoplasmic intermyofibrillar spaces, and most of the calpain and calpastatin in muscle cells is associated with intracellular structures. Immunofluorescence results suggest that concentration of m-calpain but not mu-calpain or calpastatin is, in some instances, slightly higher near the intracellular surface of the plasma membrane than elsewhere in the muscle cell. Most m-calpain, however, is distributed throughout the interior of mature rat skeletal muscle cells. Denervation, or fasting and refeeding increases the concentration of the calpains and calpastatin in the muscle cell but does not change their distribution. Some mu- and m-calpain and calpastatin is found extracellularly in denervated soleus muscle or soleus muscle from fasting rats, but the extracellular calpains and calpastatin seem to originate from "leakage" of these proteins out of the cell because serum creatine kinase levels are much higher than normal in denervated or fasting rats.

Animals↗
PubMed2005

Determination of the chronaxie and rheobase of denervated limb muscles in conscious rabbits.

Measurements of the rheobase and chronaxie can be used to define the excitability of nerves and muscles. The aim of this study was to obtain a record over many weeks of changes in the rheobase and chronaxie of denervated rabbit tibialis anterior muscle (TA). A custom-built electronic stimulator was implanted into the peritoneal cavity of New Zealand White rabbits. Large stainless steel electrodes were placed on the denervated TA muscle. Rheobase and chronaxie were measured noninvasively at weekly intervals by means of a laptop PC, which communicated with the stimulator via a radio-frequency link. At each setting the denervated TA was palpated manually to detect the response of the muscle. During the first few days after denervation the rheobase increased transiently to 0.8 +/- 0.13 mA, approximately twice the value for normal innervated muscle, then decreased to normal for the remainder of the experimental period. Chronaxie underwent a significant 3-fold increase from 4.5 +/- 1.1 ms to 14.1 +/- 1.1 ms during the first two weeks of denervation and remained elevated throughout. The custom-built implantable electronic stimulator allowed changes in muscle excitability to be studied over a long period of denervation within individual animals, providing an accurate assessment of the time course of denervation-induced changes in muscle excitability.

Analysis of Variance↗
PubMed1977

Cation movements in normal and short-term denervated rat fast twitch muscle.

1. The earliest known change in rat fast muscle following denervation is a fall in resting membrane potential unaccompanied by change in membrane resistance. The present study tested the hypothesis that increased Na permeability (P(Na)) accounted for this early depolarization.2. In all experiments, rat extensor digitorum longus muscles were studied in vitro at 25 degrees C. Li uptake in vitro, used as a measure of P(Na), was greater in 1- and 2-day denervated muscles (and in 2-day denervated diaphragm) than in paired controls.3. The extra Li taken up by denervated muscle was not sequestered in an extracellular or freely exchangeable compartment, nor was it irreversibly bound.4. Measurements of resting membrane potential and of internal Na, K, and Li in Krebs solution before and 2 hr after replacement of NaCl by LiCl, were used to compute the ratios P(Na)/P(K) and P(Li)/P(K) for normal or denervated muscles. P(Na) and P(Li) were similar relative to P(K) within each class of muscle.5. Both P(Na)/P(K) and P(Li)/P(K) ratios were elevated more than twofold in denervated muscle, as were most estimates of relative P(Li) approximated by the flux equation.6. These data, and measurement of resting membrane potential of normal muscle in 1 mM external K-Krebs solution, support the view that an electrogenic Na-K pump does not substantially contribute to this potential of normal or denervated muscle, and that the early depolarization after denervation results from increased P(Na).7. The Na-K pump of denervated muscle was as sensitive to ouabain as normal muscle. An effect of ouabain on P(Na) may explain previously noted differential effects of ouabain on normal and denervated muscle.

Animals↗
PubMed1981

[Molecular forms of acetylcholinesterase in frog skeletal muscle: effects of denervation].

In the muscles of the frog, four main molecular forms of acetylcholinesterase are present, with sedimentation coefficients of 5.7, 10.4, 13 and 17.6 S. The heaviest forms, 13 S and 17.6 S are found in both nerve-free segments and endplates zones of sartorius muscle. They decrease in long-term denervation experiments. Consequently, these two forms are not specifically localized in endplates containing regions. However, they depend either on muscle activity or on neural influence or both.

Acetylcholinesterase↗
PubMed1996

Changes in some troponin and insulin-like growth factor messenger ribonucleic acids in regenerating and denervated skeletal muscles.

To investigate the role of innervation and to determine if the process of muscle differentiation is preprogrammed, the expression of insulin-like growth factors (IGF-I and IGF-II), troponin I and troponin T mRNAs was studied in regenerating transplants of rat Extensor digitorum longus muscle in the presence and absence of nerve. The role of innervation was further investigated by denervating some adult fast (Gastrocnemius and Plantaris) and slow (Soleus) skeletal muscles. In normal adult skeletal muscles, IGF-I, IGF-II and developmental fast troponin T mRNA containing exon y, are undetectable or present at very low levels. Induction of all these mRNAs was observed in regenerating muscles in both the presence and absence of nerve as well as following denervation of adult fast and slow skeletal muscles. Their low level expression was maintained in adult denervated skeletal muscles but gradually suppressed in both innervated and noninnervated regenerating extensor digitorum longus muscle transplants after 2 months. Fast troponin T mRNA was synthesized in both innervated and noninnervated EDL transplants although the level of this transcript changed markedly in response to denervation of both adult fast and slow skeletal muscles. The fast troponin T mRNA containing exon 17 was also initially expressed in both regenerating muscles but its level was reduced with time in both transplants and in all adult denervated skeletal muscles. Fast and slow troponin I mRNAs were synthesised during EDL muscle regeneration in both the presence and absence of nerve but the slow troponin I expression was not maintained in noninnervated transplants. The level of fast troponin I mRNA decreased in denervated fast skeletal muscles but markedly increased in denervated Soleus. The level of slow troponin I mRNA was slightly increased in denervated fast skeletal muscles but considerably reduced in denervated Soleus.

Animals↗
PubMed1990

Differential effects of age on neuromuscular transmission in partially denervated mouse muscle.

The response of the neuromuscular junction to expansion of the motor unit after partial denervation (section of L5 root) was compared in soleus muscles from young (5-8 month) and old (25-30 month) mice. The object was to determine the relative capacity of young and old motor neurons to adapt to an enlarged functional field of innervation, and to delineate physiological parameters that are compromised under these conditions. Neuromuscular function was studied at 30, 60, and 120 d after partial denervation. The initial (18-23) and postoperative number (5-8) of motor units was the same in both age groups. Twitch strength declined in proportion to loss of motor units at 30 d but returned completely (young) or nearly completely (old) by 60 d. In old but not young muscle, the safety factor (assayed by twitch depression in low calcium) was decreased even before functional sprouting had occurred, indicating a reduced safety factor in nondenervated junctions. The proportion of fibers with "long" latencies (delay between stimulation and endplate potential) increased transiently (at 30 d) in young muscle but persisted without recovery at 120 d in regenerated junctions in old muscle. After partial denervation, decline in miniature endplate potential (mepp) amplitude, in mepp frequency, and in estimated quantal content of evoked release was relatively more pronounced in old than in young mice, and in the case of mepp amplitude and frequency, more persistent. Mepp amplitude was also decreased in presumed nondenervated junctions of old muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1995

Expression of utrophin and its mRNA in denervated mdx mouse muscle.

Utrophin is a large cytoskeletal protein which shows high homology to dystrophin. In contrast to the sarcolemmal distribution of dystrophin, utrophin accumulates at the postsynaptic membrane of the neuromuscular junction. Because of its localization within this compartment of muscle fibers, expression of utrophin may be significantly influenced by the presence of the motor nerve. We tested this hypothesis by denervating muscles of mdx mouse and monitoring levels of utrophin and its mRNA by immunofluorescence, immunoblotting and RT-PCR. A significant increase in the number of utrophin positive fibers was observed by immunofluorescence 3 to 21 days after sectioning of the sciatic nerve. Quantitative analyses of utrophin and its transcripts in hindlimb muscles denervated for two weeks showed only a moderate increase in the levels of both utrophin (approximately 2-fold) and its transcript (approximately 60 to 90%). The present data suggest that although utrophin is a component of the postsynaptic membrane, its neural regulation is distinct from that of the acetylcholine receptor.

Animals↗
PubMed1986

Calcium-related abnormalities in fast and slow denervated skeletal muscle in rats.

Muscle weights, Ca-ATPase activity and calcium-binding proteins were studied after denervation in rat extensor digitorum longus (EDL) and soleus (Sol) muscles. Muscle weights decreased progressively as a function of denervation time: after 28 days EDL weight diminished by 70% and Sol weight by 47%. Ca-ATPase activity and calsequestrin were quite reduced in control Sol as compared to the control EDL. Denervation caused a considerable reduction in Ca-ATPase and calsequestrin in EDL, making it resemble the control Sol.

Animals↗
PubMed2002

[The effect of MyoD family proteins on muscular atrophy induced by brachial plexus injury in rats].

OBJECTIVE: To study the changes of MyoD/myogenin expression in atrophic muscle after injury of brachial plexus among rats and to explore the role of proteins of MyoD family in denervation-induced muscular atrophy. METHODS: The brachial plexus was injured uniliterally among 24 SD rats. Then the rats were randomly divided into four groups treated by perfusion into the stomach with FGb 761 (extract of ginkgo leaf), creatine, clenbuterol, or distilled water (control group) at the dosage of 100 mg(-1).kg(-1).d(-1) for 8 weeks respectively. The changes of MyoD protein and myogenin were measured by Western blotting. The gene expression of MyoD and myogenin were determined by RT/PCR and Northern blotting. RESULTS: The expression of myogenin was upregulated within 24 hours after denervation then decreased in five days. On the seventh day, the expression of myogenin in the experimental side was weaker than in the control side. The expression of MyoD protein was downregulated soon after denervation. The expression of myogenin mRNA and MyoD was significantly downregulated after denervation. Clenbuterol, Egb, and creatine upregulated the expression of MyoD protein to a certain degree, creatine being the most effective and Egb being the least effective relatively. Clenbuterol and Egb upregulated the expression of myogenin in denervated muscle, clenbuterol being more effective. Creatine did not upregulate the expression of myogenin in denervated muscle remarkably. CONCLUSION: After denervation, the expression of MyoD protein and myogenin decreases, which plays an important role in atrophy of denervated muscle. EGb, creatine and clenbuterol retard the denervation-induced muscular atrophy by upregulating the expression of MyoD and/or myogenin.

Animals↗
PubMed1993

Comparison between the effects of botulinum toxin-induced paralysis and denervation on molecular forms of acetylcholinesterase in muscles.

Velocity sedimentation analysis of acetylcholinesterase (AChE) molecular forms in the fast extensor digitorum longus muscle and in the slow soleus muscle of the rat was carried out on days 4, 8, and 14 after induction of muscle paralysis by botulinum toxin type A (BoTx). The results were compared with those observed after muscle denervation. In addition, the ability of BoTx-paralyzed muscles to resynthesize AChE was studied after irreversible inhibition of the preexistent enzyme by diisopropyl phosphorofluoridate. Major differences were observed between the effects of BoTx treatment and nerve section on AChE in the junctional region of the muscles. A precipitous drop in content of the asymmetric A12 AChE form was observed after denervation, whereas its decrease was much slower and less extensive in the BoTx-paralyzed muscles. Recovery of junctional AChE and of its A12 form after irreversible inhibition of the preexistent AChE in BoTx-paralyzed muscles was nevertheless very slow. It seems that a greater part of the junctional A12 AChE form pertains to a fraction with a very slow turnover that is rapidly degraded after denervation but not after BoTx-produced muscle paralysis. The postdenervation decrease in content of junctional A12 AChE is therefore not primarily due to muscle inactivity. The extrajunctional molecular forms of AChE seem to be regulated mostly by muscle activity because they undergo virtually identical changes both after denervation and BoTx paralysis. The differences observed in this respect between the fast and slow muscles after their inactivation must be intrinsic to muscles.

Acetylcholinesterase↗
PubMed1998

Double crush syndrome in lower extremities.

Retrospective analysis of results of electromyography and nerve conduction velocity was performed in 169 patients with lower back pain, mostly caused by trauma. A total 289 peroneal, 280 posterior tibial and 301 sural nerves were included in statistical analysis. Peripheral entrapment of nerves (tarsal tunnel syndrome and anterior tarsal tunnel syndrome) were found in 5.3% of patients, signs of acute or chronic partial muscle denervation of corresponding muscles of lower extremities in 21.8% of patients, and abnormally prolonged F-wave latency in 12.5% of patients. Combined partial denervation and abnormally prolonged F-wave latency were found in 6.2% of patients, combined partial denervation and peripheral entrapment of nerves in 4.4% of patients, combined abnormally prolonged F-wave latency and peripheral entrapment of nerves in 2.4% of patients and combined partial denervation, abnormally prolonged F-wave latency and peripheral entrapment of nerves in 3.5% of patients. Statistical analysis of these data showed significantly higher than random overlap of peripheral entrapment syndromes and signs of proximal nerve damage of the corresponding nerves (partial muscle denervation or abnormalities of F-wave). This higher than random coincidence of the two conditions strongly suggests cause-and-effect relationship of damage of the proximal stretch of motor nerve fibers and development of peripheral entrapment syndromes in the same nerves rather than a random coincidence of two independent pathologies. Appreciation of this causal relationship is important in the development of comprehensive approach to treatment of peripheral entrapment syndromes. In appropriate cases, simultaneous treatment of the lower back problem should be considered as well.

Adolescent↗
PubMed2002

Motor denervation of tumors of the head and neck: changes in MR appearance.

PURPOSE: We reviewed the MR appearance of motor denervation of the third (mandibular) division of the trigeminal nerve (V3) and of the hypoglossal nerve. METHOD: Six cases of tumor of the head and neck with motor denervation were retrospectively evaluated. These comprised two patients with V3 denervation, three patients with hypoglossal nerve denervation, and one patient with both V3 and hypoglossal denervation. The observation was conducted for 6 to 44 months after onset. In denervated muscles, changes in signal intensity in T(1)- and T(2)-weighted images, degree of contrast enhancement, and volume of muscle were estimated during the follow-up period. RESULTS: In all cases of V3 denervation, the muscles showed no change in signal intensity in the T(1)-weighted images up to three months after onset. In two cases of hypoglossal denervation, the tongues appeared ipsilaterally hyperintense in the T(1)-weighted images within the first three months. In one case with V3 denervation and two cases with hypoglossal denervation, denervated muscles appeared hyperintense in the T(2)-weighted images up to three months after onset. At three months after denervation, the signal intensities of all motor-denervated areas increased in both T(1)- and T(2)-weighted images. Postcontrast T(1)-weighted images obtained within the first three months displayed contrast enhancement of all denervated muscles. In three cases of V3 denervation, the volumes of the affected muscles were reduced after the first three months. In three cases of hypoglossal denervation, the ipsilateral volume of the tongue decreased at three months after onset. CONCLUSION: Up to three months after onset, the denervated muscles appeared hyperintense in the T(2)-weighted images and contrast enhancement in postcontrast T(1)-weighted images before fatty infiltration and volume loss were apparent. Familiarity with the MR appearance of denervated muscles accompanying tumors of the head and neck is important to avoid confusion with inflammatory or neoplastic processes.

Adult↗
PubMed1997

Stability of myosin heavy chain isoforms in selectively denervated adult rat muscle spindles.

BACKGROUND: Rat intrafusal fibers consist of multiple isoforms of myosin heavy chains (MHCs) whose expression involves complex interactions among motor neurons, sensory neurons, and muscle cells during spindle development. Little is known about the roles of sensory and motor innervation in regulating and maintaining expression of MHC isoforms in adult rat muscle spindles. METHODS: MHC expression was investigated in deafferented or deefferented adult rat muscle spindles by reacting transverse sections of spindles with a panel of monoclonal antibodies specific for different MHC isoforms. RESULTS: Deefferentation or deafferentation did not alter the number of intrafusal fibers expressing most MHC isoforms. However, the numbers of fibers expressing two MHC isoforms were altered in deefferented muscle spindles. Nuclear bag1 fibers ceased to express alpha-cardiac MHC and upregulated embryonic MHC after ablation of motor innervation. Likewise, bag2 and chain fibers downregulated avian neonatal/fast MHC following deafferentation, but chain fibers upregulated type 2A MHC and became more extrafusal-like in their pattern of MHC expression. CONCLUSIONS: These data indicate that (1) perturbations in spindle sensory and motor nerve supplies produce less severe alterations in MHC expression in mature intrafusal fibers than do similar lesions in developing intrafusal fibers and (2) MHC expression in intrafusal fibers reflects a combination of inductive and suppressive effects of motor and sensory neurons.

Animals↗