Parvalbumin immunocytochemistry and calcium deposition in muscle fiber necrosis and subsequent regeneration following intramuscular injection of metoclopramide.

Abstract

We have studied the sequential change of parvalbumin immunocytochemistry and its correlation with intracellular Ca2+ deposition in an animal model of muscle fiber necrosis and regeneration induced by intramuscular injection of metoclopramide. Twenty-four hours after the drug's injection, extensive muscle fiber necrosis, together with dramatic loss of parvalbumin immunoreactivity and intracellular Ca2+ deposition, was observed. Muscle fiber regeneration began on day 4 after the injection and was complete by the end of the third week. Parvalbumin was not detected in the regenerating fibers, but gradually emerged during the second week as muscle fibers increased in size. It can be suggested that loss of parvalbumin in necrotic fibers is secondary to the loss in integrity of the sarcolemma. Alternatively, loss of parvalbumin in degenerating fibers may impair calcium buffering and act as a contributory factor in the necrotic process. The progressive appearance of parvalbumin immunoreactivity in regenerating fibers parallels that found in normal myogenesis.