Whole skeletal muscle transplantation: Mechanisms responsible for functional deficits

Carlson, Bruce M.; Kadhiresan, V.

doi:10.1002/bit.260430810

Cited by 15 publications

(8 citation statements)

References 22 publications

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“…Menger et al, 1992;Menger and Messmer, 1993;Hvaal et al, 1996). Damage to blood vessels and the temporary interruption of the circulation followed by ischemia causes massive cell death after the transplantation of whole skeletal muscles (reviewed by Faulkner et al, 1994).…”

Section: Abstract: Capillaries; Arterioles; Vascularization; Skeletamentioning

confidence: 99%

Remodeling of the vascular bed and progressive loss of capillaries in denervated skeletal muscle

2000

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Very little is known regarding structural and functional responses of the vascular bed of skeletal muscle to denervation and about the role of microcirculatory changes in the pathogenesis of post-denervation muscle atrophy. The purpose of the present study was to investigate the changes of the anatomical pattern of vascularization of the extensor digitorum longus muscle in WI/HicksCar rats 1, 2, 4, 7, 12, and 18 months following denervation of the limb. We found that the number of capillaries related to the number of muscle fibers, i.e. the capillary-to-fiber ratio (CFR), decreased by 88%, from 1.55 +/- 0.35 to 0.19 +/- 0.04, during the first 7 months after denervation and then slightly declined at a much lower rate during the next 11 months of observation to 10% of the CFR in normal muscle. Between months 2 and 4 after denervation, the CRF decreased by 2.4 times, from 58% to 24% of the control value. The loss of capillaries during the first 4 months following nerve transection was nearly linear and progressed with an average decrement of 4.16% per week. Electron microscopy demonstrated progressive degeneration of capillaries following nerve transection. In muscle cells close to degenerating capillaries, the loss of subsarcolemmal and intermyofibrillar mitochondria, local disassembly of myofibrils and other manifestations of progressive atrophy were frequently observed. The levels of devascularization and the degree of degenerative changes varied greatly within different topographical areas, resulting in significant heterogeneity of intercapillary distances and local capillary densities within each sample of denervated muscle. Perivascular and interstitial fibrosis that rapidly developed after denervation resulted in the spatial separation of blood vessels from muscle cells and their embedment in a dense lattice of collagen. As a result of this process, diffusion distances between capillaries and the surfaces of muscle fibers increased 10-400 times. Eighteen months after denervation most of the capillaries were heavily cushioned with collagen, and on the average 40% of the muscle cells were completely avascular. Devascularization of the tissue was accompanied by degeneration and death of muscle cells that had become embedded in a dense lattice of collagen. Immunofluorescent staining for the vascular isoform of alpha-actin revealed preservation of major blood vessels and a greater variability in thickness of their medial layer. Hyperplastic growth of the medial layer in some blood vessels resulted in narrowing of their lumens. By the end of month 7 after denervation, large deposits of collagen around arterioles often exceeded their diameters. Identification of oxidative muscle fibers after immunostaining for slow-twitch myosin, as well as using ultrastructural criteria, has shown that after 2 months of denervation oxidative muscle fibers were less susceptible to atrophy than glycolytic fibers. The lower rate of atrophy of type I muscle fibers at early stages of denervation may be explained by their initially bette...

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Section: Abstract: Capillaries; Arterioles; Vascularization; Skeletamentioning

confidence: 99%

Remodeling of the vascular bed and progressive loss of capillaries in denervated skeletal muscle

2000

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“…41,42 In contrast, available data suggest that, under many circumstances, denervation/reinnervation and tenotomy and repair can result in deficits in skeletal muscle contractile function. 16,18,26,[43][44][45] These factors must remain the prime independent variables in future studies of mechanical function in neurovascular muscle transfer.…”

Section: Discussionmentioning

confidence: 99%

“…Second, available experimental evidence suggests that, under most circumstances, muscles with many regenerated fibers manifest a deficit in mechanical function. 26,31 Note that, although available evidence suggests that intraoperative ischemia times less than 3 hours in duration do not correlate with the recovery of muscle function after microneurovascular transfer, 13 this evidence does not preclude the possibility that ischemia-induced degeneration and regeneration of individual muscle fibers results in a population of muscle fibers with suboptimal mechanical function. As a result, a longstanding hypothesis in this area of research has been that muscle fiber degeneration and regeneration may account, at least partially, for the mechanical dysfunction in muscle after neurovascular transfer.…”

mentioning

confidence: 96%

“…3,[13][14][15][16][17][18][19][20][21][22][23][24] The mechanisms responsible for muscle mechanical dysfunction after neurovascular transfer have not been fully determined. 25,26 In vivo, death of individual muscle fibers is followed by a well-described process of muscle fiber degeneration and regeneration. [27][28][29] Degeneration and regeneration of skeletal muscle fibers has been proposed as a mechanism contributing to the mechanical deficit in neurovascular muscle transfers for two reasons.…”

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confidence: 99%

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Neurovascular Transfer Does Not Cause Skeletal Muscle Fiber Degeneration

Demeester¹,

Hasan²,

Urbanchek³

et al. 2006

Plastic and Reconstructive Surgery

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“…The total mass of the regenerating tissue is one of the most important determinants of successful regeneration. Faulkner et al concluded that the upper limit of tissue mass that permits muscle regeneration after grafting is approximately 6 g. 46 The authors speculated that failure of larger grafts to regenerate arose from difficulties with revascularization and reinnervation of the regenerating transplant. This explains why muscle grafts recover significantly better in small animals than in mammals possessing large body sizes.…”

Section: Regenerative Responses In Skeletal Muscle Of Different Mammamentioning

confidence: 99%

Regeneration of skeletal and cardiac muscle in mammals: do nonprimate models resemble human pathology?

Borisov

1999

Wound Repair Regeneration

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Most of the available information regarding the regenerative potential and compensatory remodeling of mammalian tissues has been obtained from nonprimate animals, mainly rodent experimental models. The increasing use of transgenic mice for studies of the mechanisms controlling organogenesis and regeneration also requires a clear understanding of their applicability as experimental models for studies of similar processes in humans and other mammals. Application of modern cell biology methods to studies of regenerative processes has provided new insights into similarity and differences in cellular responses to injury in the tissues of different mammalian species. During more than 200-million years of progressive divergent evolution of mammals, cellular mechanisms of tissue regeneration and compensatory remodeling evolved together with increasingly adaptive functional specialization and structural complexity of mammalian tissues and organs. Rodents represent a phylogenetically ancient order of mammals that has conservatively retained a number of morphofunctional characteristics of early representatives of this class, which include enhanced regenerative capacity of tissues. A comparative analysis of regenerative processes in skeletal and cardiac muscle, as well as in several other mammalian tissues, shows that time courses and intensities of regeneration in response to the same type of injury vary even within taxonomically related species (e.g., rat, mouse, and hamster). The warm bloodedness of mammals facilitated the development of more complex mechanisms of metabolic, immune, and neurohumoral regulation, which resulted in a stronger dependence of regenerative processes on vascularization and innervation. For this reason, interspecies modifications of regenerative responses are limited by the capacity of the animal to resorb rapidly the foci of necrosis and to revascularize and reinnervate the volume of the regenerating tissue. These differences, among other factors, result in significantly lower rates of reparative regeneration in mammals possessing larger body sizes than rodents. A review of these data strongly indicates that the phylogenetic age and biological differences between different species should be taken into account before extrapolation of regenerative properties of nonprimate tissues on the regenerative responses in the primates.

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Whole skeletal muscle transplantation: Mechanisms responsible for functional deficits

Cited by 15 publications

References 22 publications

Remodeling of the vascular bed and progressive loss of capillaries in denervated skeletal muscle

Remodeling of the vascular bed and progressive loss of capillaries in denervated skeletal muscle

Neurovascular Transfer Does Not Cause Skeletal Muscle Fiber Degeneration

Regeneration of skeletal and cardiac muscle in mammals: do nonprimate models resemble human pathology?

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