Leo C. Massopust

Effects of use and disuse on nerve endings, neurosomes, and fiber types in skeletal muscle.

Summary The limited experimental evidence presented in this paper tends to support the following statements: The normally used and innervated gastrocnemius muscle of the white rat is characterized histologically by dark, coarsely granular and light, finely granular and agranular muscle fibers. The nerve endings are usually retracted in the dark, coarsely granular fiber and expanded in the light, agranular fiber, as revealed by gold impregnation of teased whole muscle fibers. The atrophy of disuse following tenotomy of the gastrocnemius muscle with nerve supply intact, is accompanied, during the first month, by the progressive loss of the narrow and dark, coarsely granular muscle fiber, and by a depletion of its innervation. The dark, granular muscle fiber is determined by the reciprocal interaction of the normally intact and attached muscle fiber with its normally functioning innervation. During the process of atrophy of disuse after tenotomy, small and giant fusiform neurosomes are discharged from the altered nerve endings. It is assumed that these giant fusiform neurosomes are the product of a retardation in the rate of the discharge, diffusion, and disappearance by hydrolysis, following tenotomy and disuse atrophy of the innervated gastrocnemius muscle. There appears to be a parallelism between the atrophy by disuse of tenotomized muscle and the loss of the normal discharge of neurosomes from the altered and progressively depleted innervation of the muscle. One factor in the atrophy of disuse of muscle appeared, therefore, to be the substantial loss of the discharge of neurosomes into muscle as well as the quantitative decrease of the myoplasm. The giant fusiform neurosomes that appear during the early period following tenotomy disappear when the living muscle in situ is adequately restretched prior to excision and gold impregnation.

Acute Anatomic Breakdown of Motor End Plates in Hemorrhagic Shock.

Summary The limited evidence in this paper supports the claim that hemorrhagic shock profoundly alters the morphology of the motor end plates and finally produces loss of structural innervation of many muscle fibers in a single voluntary muscle. This histologic change is highly irregular in the different muscles of the rat, therefore large numbers of specimens from different muscles were teased. Gold staining masses of axonic materials drain out into and between the muscle fibers coincident in time with the loss of motor innervation due to the increased permeability of the end plates. The epilemmal axons, exhausted of their substances, are in many places likewise denuded of their hypolemmal end plates. There is therefore a real anatomic breakdown of many motor end plates and histologic alteration of certain skeletal muscles in hemorrhagic shock.

Sudden Destruction of Motor End Plates by Lactic Acid

Summary Lactic acid in concentrations of 0.05 to 0.3% injected into the exposed zone of innervation of the sternomastoid muscle in the white rat produced sudden destruction of most of the motor end plates within 30 seconds to 25 minutes dependent upon the concentration of the acid. This liquefaction of the hypolemmal axons of the end plates was preceded by a first phase of retraction and a second phase of expansion and fragmentation. Lactic acid caused a progressive depletion, in both the hypolemmal and the epilemma1 axons, of auriphilous substances. The blood vessels were enlarged, hyperemic, and contained clumps of agglutinated red blood cells in the rigorous muscle paralyzed by lactic acid. I t is suggested that the acid metabolites which accumulate during rigor mortis of muscle are responsible for the destruction of the end plates and that during life certain processes that result in the intramuscular accumulation of acid, such as vascular congestion and anoxia, likewise may result in the destruction of the motor end plates.

Exaggerated Discharge of Neurosomes into Spastic Muscle by Heat Reflex.

Summary The limited experimental evidence presented tends to support the statement that the reflex effects of heat applied to the skin are associated with the exaggerated discharge of ephemeral, pleomorphic, and lipoidal neurosomes from the motor end plates into spastic or cramp-like muscle. The neurosomes have a variable affinity for gold, silver, and lipoidal stains. There are characteristic instantaneous changes in the morphology of the motor end plates and myoplasm in response to the reflex effects of thermal trauma applied to the skin.