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.

Basic Appl Myol 11 (2): 75-85, 2001

 

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.

Basic Appl Myol 11 (2): 87-90, 2001

 

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.

Basic Appl Myol 11 (2): 91-98, 2001

 
 

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.

Basic Appl Myol 11 (2): 99-104, 2001

 
 

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.

Basic Appl Myol 11 (2): 105-110, 2001