Abstract
An electron-microscopic study on dystrophic chicken white muscle, posterior latissimus dorsi (PLD), was performed with histochemical identification of three fiber types of βR (red), αR and αW (white) fibers to evaluate the pathophysiology in fiber necrosis. As seen in histochemically stained sections, vacuolar formation in the cytoplasm, an outstanding pathologic feature in chicken dystrophy, was recognized in the αW fibers by electron microscopy. The vacuole was membrane-bound and thought to originate from coalescence or dilatation of extensively proliferated sarcotubular system. There was evidence of a delay in fiber type transformation from αR to αW in dystrophic white muscle, while the initial pathologic event of sarcotubular system proliferation might be expressed only after muscle fibers had attained histochemical characteristics of αW fibers. Localized myofibrillar degeneration was encountered in the vicinity of the vacuole with focal membrane defect. An influx of extracellular fluid through the vacuolated sarcotubular system into the sarcoplasm may activate certain proteases, such as calcium-dependent protease because the extracellular fluid contains high concentration of calcium ion. The activated protease then degrades structural protein, especially Z-line protein, followed by fiber necrosis with phagocytosis.