PHARMACOLOGICAL STUDIES ON FIBRILLATION VOLTAGES IN DENERVATED SKELETAL MUSCLE OF RABBIT

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The effects of various drugs on fibrillation in chronically denervated skeletal muscles of rats were studied by Brown (1937) (1) and Solandt and Magladery (1940) (2), and they reported that the fibrillation may be prevented by the administration of quinidine and acetylcholine (ACh) but not by that of ether, sodium barbitone, atropine, eserine and curare. Furthermore, McIntyre, King and Dunn (1945) (3) and Jarcho, Berman, Eyzaguirre and Lilienthal (1951) (4) reported that ACh, decamethonium and d-tubocurarine aroused an almost immediate outburst of electrical fibrillary activity, rapidly followed by complete silence in denervated mammalian muscles and the effect of ACh on the denervated muscle may be inhibited by the previous injection of sufficient doses of d-tubocurarine. It is said that fibrillation is a physiological response of skeletal muscle to denervation and is accompanied by action potentials referred to as fibrillation voltages. Denny-Brown and Pennybacker (1938) (5) found that chronically denervated skeletal muscle undergoes certain degenerative changes and produces the action potentials spontaneously. Golseth and Fizzell (1947) (6) investigated in detail the fibrillation action potentials, which may be either monophasic or diphasic in character, and found them to be 2 to 30 c/s in frequency, 10 to 100 μV in potential and 1 to 2 msec in duration. Cannon and Rosenblueth (1949) (7) pointed out that the chronically denervated skeletal muscle becomes much more sensitive to ACh than the normal muscle. Moreover, ThesleE (1960) (8) reported that the whole surface of denervated muscle fiber is as sensitive to ACh as the end-plate region which has maintained its responsiveness to it. The mechanism of the development of the fibrillation voltages has not been sufficiently clarified yet, although Woodbury and Ruch (1960) (9) explained that the circulating ACh is the probable cause of the fibrillation voltages. In our laboratory, the effects of various drugs including nicotine and l-1, 2-diphenyl-l-ditmethylaminoethane (Spa) on the fibrillation voltages were studied to get a clue toward solution of the following problems: whether or not the circulating ACh is the stimulating substance producing the spontaneous action potentials in the chronically denervated skeletal muscle, and whether or not Spa acts directly on the skeletal muscle membrane.
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PHARMACOLOGICAL STUDIES ON FIBRILLATION VOLTAGES IN DENERVATED SKELETAL MUSCLE OF RABBIT

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