BAM 11 (2), 2001
Table of Contenst
Review 75 Skeletal Muscle Pathology After Spinal Cord Injury.
Our 20 year experience and results on skeletal muscle
changes in paraplegics,
related to functional rehabilitation.
R Scelsi [Full text pdf 1.82Mb]
Articles 87 Enhancement of Tibialis Anterior Recovery by
Intermittent Sequential Pneumatic Compression of the Legs
A Wiener, J Mizrahi and O Verbitsky
[Full text pdf 127Kb]
91 Effects of Long-Term Stimulation on Skeletal Muscle
Phenotype Expression and Collagen/Fibrillin
Distribution
DR Trumble, C Duan and JA Magovern [Full text pdf 1.34Mb]
99 Induction of Differentiation of Adipofibroblasts
Using a Defined Treatment Medium without DMI
JL Vierck, D Dal Porto and MV Dodson
[Full text pdf 471Kb]
Skeletal Muscle Pathology after Spinal Cord Injury: Our 20 Year Experience and Results on Skeletal Muscle Changes in Paraplegics, Related to Functional Rehabilitation
Roberto Scelsi
Department of Human and Hereditary Pathology, University of Pavia, Pavia, Italy
Abstract
The present review on 20-year-experience on paralyzed skeletal
muscle in paraplegics after traumatic spinal cord injury (SCI),
reports changes in muscle fibres and microvasculature seen after
morphological, morphometric and ultrastructural studies on open
and needle biopsies. The changes were correlated with the time
elapsed from SCI (1-17 months). Histopathological and
enzyme-histochemical changes in muscle fibres were seen first
after 1 month and increased thereafter. In all stages post SCI,
paraplegics showed myopathic alterations, increase in the
sarcoplasmic lipid contents and incidental denervation patterns.
The main ultrastructural changes regard the myofibrillar apparatus
and mitochondria. Probably a fibre type shifting to type 2 fibres
occurs precociously, but only 7-8 months after SCI it is well
manifested. The blood vessel qualitative and quantitative changes
in paraplegics regard small vessels and capillaries and they may
be important causes of the myopathic alterations in paraplegics.
The influence of disuse and spasticity on morphological fibre and
capillary modifications in paraplegics is reviewed and discussed.
The knowledge of the muscle condition and of plastic capacities
for fibre type shifting in paraplegics is important to oppose
complications of SCI and to choice of an appropriate
rehabilitative program directed to prevention of changes
associated to disuse, spasticity and vascular damage.
Key words: fiber types, microvasculature, mitochondria,
MHC, pathology, skeletal muscle, spinal cord injury.
Enhancement of Tibialis Anterior Recovery by Intermittent Se-quential Pneumatic Compression of the Legs
Avi Wiener, Joseph Mizrahi(1) and Oleg Verbitsky(1)
Department of Occupational Medicine, Rambam Medical Center and (1) Department of Biomedical Engineering, Technion, Israel Institute of Technology, Haifa, Israel
Abstract
In this study we examined the effect of Intermittent Sequential
Pneumatic Compression (ISPC) of the legs on the recovery of
fatigued Tibialis Anterior (TA) muscles. Eight sub-jects performed
10 min fast walking on a treadmill, followed by 2 min sustained
effort of the TA (load A). Immediately afterwards they took 3 min
of resting time, during which one leg was treated by ISPC (active
recovery) and the opposite one served as a control (passive
recovery). A second sustained effort (load B), similar to load A
in intensity and duration, followed the recovery period. Surface
EMG of the TA was used to monitor muscle fatigue. The results
indicate that the mean power frequency (MPF) of the actively
recovering TA was significantly higher than that of the passively
recovering TA, irrespective of the side on which ISPC was applied.
An additional interesting result was the higher MPF in the
begin-ning of load B compared to that of the end of load A.
However, this difference was signifi-cant in the actively
recovering leg, but not so in the passively recovering leg. It was
conclu-ded that ISPC treatment of fatigued muscle after a
sustained effort improves its contractile capacity in comparison
to passive recovery.
Key words: fatigue, intermittent sequential pneumatic
compression, mean power fre-quency, recovery, water evacuation.
Effects of Long-Term Stimulation on Skeletal Muscle Phenotype Expression and Collagen/Fibrillin Distribution
Dennis R. Trumble, Changping Duan, and James A. Magovern
Cardiothoracic Surgery Research, Allegheny-Singer Research Institute, Depart-ment of Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania
Abstract
The effects of chronic electrical stimulation on muscle fiber
phenotype and metabolism are well known, but its impact on the
extracellular matrix is poorly understood. Material pro-perties of
skeletal muscle are largely influenced by the viscoelastic
properties of connective tissues which occupy the interstitium.
Changes in collagen and fibrillin content may therefo-re play a
key role in muscular adaptation processes. Latissimus dorsi (LD)
of eight rabbits were used to study muscular adaptation to
long-term electrical conditioning. Muscles were conditioned using
burst stimuli delivered over 6 or 12 weeks. Contralateral LD were
used as control. Stimulation produced marked reductions in maximum
isometric force, but impro-ved endurance capacity due to increased
percent cross sectional area (CSA) occupied by slow-twitch
oxidative muscle fibers. Stimulation also increased percent CSA
occupied by type I collagen and fibrillin. In contrast, the amount
of type III collagen and fast-twitch gly-colytic fibers decreased
in stimulated muscle. These data suggest that muscular adaptation
to long-term stimulation includes both alterations in fiber type
expression and remodeling of the extracellular matrix.
Key words: collagen, extracellular matrix, fibrillin,
skeletal muscle, stimulation.
Induction of Differentiation of Adipofibroblasts Using a Defined Treatment Medium without DMI
Janet L. Vierck, Dessa Dal Porto, and Michael V. Dodson
Department of Animal Sciences, Washington State University, Pullman, Washing-ton, USA
Abstract
The induction of differentiation of fat cell precursors in vitro
has traditionally been accom-plished by exposure of the cells at
confluence to a mixture of dexamethasone,
1-methyl-3-isobutylxanthine, and insulin (DMI). In our laboratory,
we treated ovine adipofibroblasts with three different defined
media to determine which one would optimize the induction of
differentiation without using DMI. A defined medium containing
insulin, transferrin, triio-dothyronine and hydrocortisone (ITTC)
promoted the most differentiation in the cultured cells.
Subsequently, we utilized ITTC to investigate the effects of
plating density, substra-tum and the timing of treatment
application on subsequent lipid conversion of ovine
adipo-fibroblasts. Two protocols resulted in similar levels of
differentiation: (1) plating at a den-sity of 20,000 cells per
well and allowing the cells to proliferate to confluence in a
serum-containing medium before the application of ITTC or (2)
plating at a density of 100,000 cells per well and adding the ITTC
treatment immediately after a 24 hour attachment period in a
serum-containing medium. Coating the wells with a substratum of
pig skin gelatin be-fore plating resulted in a small increase in
the amount of differentiation over that seen in uncoated wells. A
preliminary study testing the effect of a thiazolidinedione
(T-174) on subsequent lipid production in adipofibroblasts
determined that this chemical enhances dif-ferentiation. These
studies suggest that an optimal defined treatment medium can be
for-mulated without DMI to induce the differentiation of
adipofibroblasts to adipocytes.
Key words: adipocytes, adipofibroblasts, defined media,
differentiation, preadipocytes.
Does Normal Nitric Oxide Synthase Prevent Pathologic Muscle Changes in Dystrophin Deficiency?
Irena Niebroj-Dobosz(1, 2), Anna Fidziaska(2), Zofia Glinka(1) and Irena Hausma-nowa-Petrusewicz(2)
(1) Department of Neurology, Medical University, and (2) Neuromuscular Unit, Medical Research Center, Polish Academy of Sciences, Warsaw, Poland
Abstract
Neuronal nitric-oxide synthase (nNOS) is a member of the
dystrophin-associated proteins, re-gulates homeostasis of reactive
free radical species and may contribute to oxidative damage to
proteins in muscle diseases. To test the hypothesis that nNOS
activity may be involved in spa-ring from muscle pathology in
dystrophin deficient muscles we examined nNOS immunoreac-tivity in
muscles from Duchenne muscular dystrophy (DMD) and Becker muscular
dystrophy (BMD). The results were compared to nNOS in dystrophin
positive limb-girdle dystrophy (LGMD) patients. Similar studies in
dystrophin deficient hind limb muscles and diaphragm of clinically
almost asymptomatic mdx mice were performed. In the DMD patients
nNOS appea-red to be either drastically reduced, or absent. In BMD
and LGMD it was decreased, or nor-mal. In mdx mice muscles no
changes in nNOS immunoreactivity were present. In the
immu-nocytochemical examination in DMD nNOS was either not
stained, or the staining was obser-ved in the surrounding
connective tissue. In BMD nNOS staining was decreased or absent,
in LGMD it appeared in the muscle cell cytoplasm. In mdx mice
muscles nNOS reactivity was observed on the surface of the muscle
fiber, starting from 30 days of age of the animals clusters of
nNOS positive cells were observed.
It is suggested that the decrease of nNOS content in
dystrophinopathies is contributing to oxi-dative damage to muscle
proteins, which enhances the degeneration of the muscle fibers.
Normal nNOS may be one of factors, which prevent pathological
muscle changes in mdx mice muscles. Regulations of the activity of
this enzyme may be one of the possible strate-gies in dystrophy
treatment.
Key words: dystrophinopathies, mdx mice, nNitric oxide
synthase, oxidative damage.