TY - JOUR
T1 - Effects of percutaneous electrical stimulation on functional ability, plasma creatine kinase, and pectoralis musculature of normal and genetically dystrophic chickens
AU - Hudecki, Michael S.
AU - Caffiero, Alfred T.
AU - Gregorio, Carol C.
AU - Pollina, Catherine M.
N1 - Funding Information:
The breast musculature of genetically dystrophic Line 4 13 and genetically related normal Line 412 chickens were treated in three separate trials with high-frequency electrical stimulation (ES). Beginning on days 7 or 14 ex ovo, each bird received three ES treatments per week. Each stimulation cycle repeated five times per day consisted of 15 s “on” followed by 50 s “off.” In the third trial only, the birds were additionally treated beginning day 3 ex ovo with either leucine (100 mg/kg) or the proteinase inhibitor Ep475 (10 mg/kg). ES significantly delayed the onset of righting disability in the dystrophic chickens. However, this improvement was temporary and could be masked by single treatments of either leucine or Ep475. Plasma creatine kinase activities were increased generally in both the stimulated normal and dystrophic Abbreviations: ES-electrical stimulation, CK-creatine kinase. ’ This study was supported by grants to M.S.H. from the Task Force on Drug Development of the Muscular Dystrophy Association, the National Institute of Neurological and Communicative Disorders and Stroke (NS 16219), and a Biomedical Research Support Grant to SUNY at Buffalo from the U.S. Public Health Service. Dr. Hudecki is a Research Career Development Award recipient of NINCDS (NS 005 17). The authors are grateful to Diane Honor, Paul Schenkel, Gil Schnorr, Brett Johnson, Helen Moore, and Stephen Povoski for their technical assistance; to Dr. Reid Heffner, Andrew Koenig, and Reginald Gaudino for carrying out the histological preparations; Dr. Harvey A. Berman and Mildred Decker for assistance in the acetylcholinesterase assays; Dr. John Martner for developing the computer program for the image-analysis; James A. Stamos for his preparation of the illustrations; and Dr. Richard R. Almon for his critique and encouragement in this study. In addition a particular thanks goes to Mr. William DeVries, Vice-President, NuMed Surgical Corporation, Joliet, Illinois for loan of the Electrostim 180. Please send reprint requests to Dr. Hudecki, Department of Biological Sciences, SUNY, Buffalo, NY 14260.
PY - 1985/10
Y1 - 1985/10
N2 - The breast musculature of genetically dystrophic Line 413 and genetically related normal Line 412 chickens were treated in three separate trials with high-frequency electrical stimulation (ES). Beginning on days 7 or 14 ex ovo, each bird received three ES treatments per week. Each stimulation cycle repeated five times per day consisted of 15 s "on" followed by 50 s "off." In the third trial only, the birds were additionally treated beginning day 3 ex ovo with either leucine (100 mg/kg) or the proteinase inhibitor Ep475 (10 mg/kg). ES significantly delayed the onset of righting disability in the dystrophic chickens. However, this improvement was temporary and could be masked by single treatments of either leucine or Ep475. Plasma creatine kinase activities were increased generally in both the stimulated normal and dystrophic birds. In two trials ES increased the relative muscle mass, and in one trial increased protein. ES had little effect on normal muscle mass or protein. However, ES treatment together with either leucine or Ep475 appeared to improve both normal and dystrophic muscle mass and protein. Furthermore ES decreased dystrophic muscle calcium but not acetylcholinesterase activity. On the other hand, ES had no effect on the total normal muscle calcium but increased normal acetylcholinesterase values. In both normal and dystrophic muscle samples, ES treatment in combination with leucine appeared to increase the mean muscle fiber diameters and number of myonuclei, and in the case of the dystrophic muscle, appeared to decrease the relative proportion of vacuolated, degenerating, and intensely oxidative histochemical fibers. In general, stimulation (especially in combination with leucine) appears to alter in varying degrees the phenotypic expression of the muscle disease exhibited in the dystrophic chicken.
AB - The breast musculature of genetically dystrophic Line 413 and genetically related normal Line 412 chickens were treated in three separate trials with high-frequency electrical stimulation (ES). Beginning on days 7 or 14 ex ovo, each bird received three ES treatments per week. Each stimulation cycle repeated five times per day consisted of 15 s "on" followed by 50 s "off." In the third trial only, the birds were additionally treated beginning day 3 ex ovo with either leucine (100 mg/kg) or the proteinase inhibitor Ep475 (10 mg/kg). ES significantly delayed the onset of righting disability in the dystrophic chickens. However, this improvement was temporary and could be masked by single treatments of either leucine or Ep475. Plasma creatine kinase activities were increased generally in both the stimulated normal and dystrophic birds. In two trials ES increased the relative muscle mass, and in one trial increased protein. ES had little effect on normal muscle mass or protein. However, ES treatment together with either leucine or Ep475 appeared to improve both normal and dystrophic muscle mass and protein. Furthermore ES decreased dystrophic muscle calcium but not acetylcholinesterase activity. On the other hand, ES had no effect on the total normal muscle calcium but increased normal acetylcholinesterase values. In both normal and dystrophic muscle samples, ES treatment in combination with leucine appeared to increase the mean muscle fiber diameters and number of myonuclei, and in the case of the dystrophic muscle, appeared to decrease the relative proportion of vacuolated, degenerating, and intensely oxidative histochemical fibers. In general, stimulation (especially in combination with leucine) appears to alter in varying degrees the phenotypic expression of the muscle disease exhibited in the dystrophic chicken.
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U2 - 10.1016/0014-4886(85)90040-8
DO - 10.1016/0014-4886(85)90040-8
M3 - Article
C2 - 3876237
AN - SCOPUS:0022197161
SN - 0014-4886
VL - 90
SP - 53
EP - 72
JO - Experimental Neurology
JF - Experimental Neurology
IS - 1
ER -