Marianne Goettsch

Effect of Nerve Section upon Development of Nutritional Muscular Dystrophy in Young Rats

It is now well established that the young of female rats maintained on a diet restricted in Vitamin E, develop, towards the end of lactation, severe degeneration of the skeletal muscles. The pathological changes have been described in detail by Olcott, 1 by Pappenheimer, 2 and by Telford, Emerson and Evans. 3 Barrie 4 and Olcott found no abnormalities of the nerves, spinal cord or brain, and the spinal cord changes described by Lipschutz 5 in young rats on E-deficient diet, have not been present in our material. We have noted that even the terminal neurites and motor end plates are well preserved in the midst of the degenerating muscle fibers. Although the histological evidence thus favors a “primary my-opathy” as against a neural origin of the muscle lesions, so little is known of the pathogenesis of this disease that it seemed of interest to ascertain whether the muscle degeneration would be affected by the removal of nervous impulses. Muscular dystrophy was induced in young rats according to the technic described by Goettsch and Ritzmann. 6 Under ether anesthesia, the left sciatic nerve was sectioned through an incision on the posterior surface of the thigh, a segment several mm in length being excised. The operation was performed on various days during the lactation period—the earliest at 5 days, the latest at 18 days. The animals were killed soon after the development of symptoms, or when these were not manifest, upon the 24th day. It has been our experience that muscle lesions may be found in rats which have shown no clinical evidence of the disease. The operation was performed upon 42 rats, of which 29 developed the disease.

Transmission of nutritional muscular dystrophy to rabbits in utero.

When young rabbits are placed upon muscle-dystrophy producing Diet 11, the majority die within a period of several months. 1 Rarely the disease runs a protracted course; the animals may survive for a year, only to succumb eventually with characteristic degeneration of the skeletal muscles. One such adult dystrophic rabbit successfully completed gestation and gave birth to living young. This exceptional event, has permitted us to observe that nutritional muscular dystrophy may be passed on from mother to offspring. Rabbit 241 was born in the laboratory on Jan. 15, 1935. On Feb. 19th, it was weaned and given Diet 11.∗ A biopsy from the thigh muscles was taken on Jan. 6th, 1936, when the animal had attained a weight of 2.4 kilos. A few necrotic fibers were found in each low power field. The muscle creatin was 540 mg.—within the normal range. Two subsequent biopsies on Nov. 19th and Dec. 11th showed little progression of the lesions. On Jan. 7th, 1936, she was mated with a stock breeding male, which was known to have sired several normal litters, and which had been maintained on a stock diet of grains and alfalfa. On Feb. 8th, Rabbit 241 gave birth to a litter of 2. The young seemed somewhat scrawny, but they were not carefully examined for fear of disturbing the mother. The following morning, the newborn rabbits were found dead. Their skeletal muscles at autopsy were strikingly pale. No other pathological change was recorded. Histologically, sections taken from various muscles all showed extreme lesions (Fig. 1). Many of the fibers—in some field almost 50%—were undergoing hyaline necrosis, with segmentation and rupture. They were widely separated by an œdematous stroma in which were great numbers of elongate fusiform cells with vesicular nuclei and basophilic cytoplasm.

Protection Afforded by Certain Vegetable Oils against Nutritional Encephalomalacia of Chicks.

For several years, attempts have been made to protect chicks against nutritional encephalomalacia 1 (1) by supplementing Diet 108† with various natural foodstuffs; (2) by varying the proportion of the ingredients. A summary of these experiments is given in Table I. Although there have been indications that the addition of certain foodstuffs such as wheat, corn, lettuce, spinach and grass conferred partial protection, the results have been by no means consistent. Various modifications in the proportion of the mineral and organic ingredients of Diet 108 have likewise failed to induce complete protection. It has been noted that reduction of the lard content regularly lowers the incidence of the disease, but even complete omission of lard from the diet does not give absolute protection. This indicates that the disease is not due primarily to toxicity of the lard. When certain vegetable oils were substituted for lard in Diet 108, all the chicks remained free from the disease. Experiments demonstrating this are presented in Table II. Thus far Crsco, Wesson Oil, Mazola and peanut oil at the level of 20% have afforded complete protection. Olive oil has been less efficacious. Fractionation of these oils is now being carried out in the attempt to gain further knowledge as to the nature of the protective factor.