Abstract
The thesis that atrophy, such as occurs in normal involutionary tissue absorption, in muscle whose nerve supply has been severed, etc., involves a change either in autolytic enzyme content or in its activation, is not supported by experiments of the writer. It has been shown by him 1 that in the larval frog, where, during metamorphosis extensive atrophy occurs, the histological picture resembles closely those of polymyositis, dermatomyositis, etc., as described by Strümpell, Jacoby, Steiner, et al., and that in the case of this amphibian, there is no acceleration of autolysis in vivo nor in vitro and where thyroid is used to accelerate metamorphosis, as Gudernatsch first showed, the time of completion of the process is reduced two thirds; even in this case, there is no change in rate of autolysis. In another set of experiments, the left sciatic of a rabbit was cut under asepsis, the wound healing, as far as it was permitted to go, without bacterial interference; after a week, the muscles affected were compared as to power for autolysis in vitro after the method of Salkowski and here, again, no acceleration of rate of enzyme action was determined.
I know of but a few citations in biochemical literature to investigations along these lines. All of these 2 seem to bear out the same conclusion. Grund, for instance, in an experiment similar to the one above, found the ratio residual nitrogen to total nitrogen to be less than one, and while residual nitrogen involves more than products of hydrolysis of muscle proteins, yet the point is significant; at least there is no increase in tannic acid non-precipitable nitrogen as one would certainly postulate if autolysis is increased in atrophying muscle.
Get full access to this article
View all access options for this article.
