524 THE TOCOPHEROLS 



protects against dystrophy. ^^ Death is usually ascribed to serious impair- 

 ment of the respiratory musculature, but other metabolic dysfunctions 

 may be involved. The following description is based upon the reports of 

 Olcott/^ Telford et al.,^'" Pappenheimer,^^' ^^- " and Mason"^ 



Grossly, the skeletal muscles are pale, ischemic, moist, and sometimes 

 grayish and gritty owing to calcium deposition. Microscopically, there is 

 widespread interstitial edema, leucocytic infiltration and segmental frag- 

 mentation of muscle fibers (Fig. 2). The affected segments show loss of cross 

 striations, amitotic proliferation of sarcolemma nuclei, hyaline necrosis of fi- 

 brillar substance, nuclear fragmentation, rupture of sarcolemma sheaths, and 

 removal of debris by invading macrophages. In the densely cellular areas 

 marking the point of breakdown of fiber segments, there appear many baso- 

 philic, fusiform, or band-like strands with centrally located nuclei; these 

 represent young, regenerating fibers presumably ai'ising from plasmodial 

 masses and, perhaps, from intact muscle nuclei with investing sarcoplasm 

 released in the degenerative breakdown of the fibers (Fig. 3). Edema and leu- 

 cocytic infiltration diminish in a few days, and regenerating fibers become 

 increasingly numerous. The frequent presence of a layer of normal fibers 

 at the periphery of the muscle suggests that proximity to good vascular 

 supply may retard the dystrophic process. ^^' ^^ 



Weanling rats low in E but exhibiting no symptoms of paralysis, and 

 rats showing spontaneous recovery from paralysis, usually show consider- 

 able muscle damage histologically.^^' ^^ Similar muscle changes, unassoci- 

 ated with external symptoms, have been observed in newborn rabbits,^^ 

 in prepubertal mice," and in young pigs.^^^ The muscular dystrophy ob- 

 served in "stiff-lamb" disease,^^- ^^' ^"'^ in "white muscle disease" of young 

 calves,*^ and in a similar syndrome in the foal,^' all of which occur under 



53 A. M. Pappenheimer, /. ML Sinai Husp. N. Y. 7, 65 (1940); Physiol. Revs. 23, 37 



(1943). 

 " H. S. Olcott, J. Nutrition 15, 221 (1938). 

 55 I. R. Telford, G. A. Emerson, and H. M. Evans, Proc. Sac. Exptl. Biol. Mnl. 41, 



291 (19.39): 45, 135 (1940). 

 5« A. M. Pappenheimer, Am. J. Pathol. 15, 179 (1939). 

 " A. M. Pappenheimer, On Certain Aspects of Vitamin I". Deficiency, American 



Lecture Series No. 17, Charles C Thomas, Sprinfi;hehl, 111., 1948. 

 "»K. E. Mason, Proc. 1st & 2nd Med Conf. (1951-52) Muscular Dystr. Ass'ns Amer., 



New York p. 94. 

 58 J. P. Willman. S. A. Asdell, and P. Olafson, (\>niell Ayric. E.rp. Sla. Bull. 603, 3 



(1934). 

 59.J. P. WiUmaii, J. K. Loosli, S. A. Asdell, F. B.Morrison, and P. Ohit'son, ./. Animal 



Sci. 4, 128 (1945); Cornell Vet. 36, 200 (1946). 

 s"'' H. H. Draper, M. F. James, and B. C. Johnson, ./. .Xutrition 47, 5S3 (1952). 

 6» L. R. Vawter and E. Records, ./. Am. \'(t. Mai. .l.ssor. 110, 152 (1947). 

 " T. C. Jones and W. O. Reed, ./. .1///. \'ct. .Med. Assoc. 113, 170 (1948). 



