Studies on the pathogenesis of the myopathy of coffee senna (Cassia occidentalis) poisoning in rabbits

Abstract

The pathogenesis of the myodegeneration of striated muscles of rabbits poisoned with coffee senna (Cassia occidentalis L.) was studied by use of routine pathological methods. The heart was enlarged due to dilatation of all chambers and the myocardium was pale or yellow. The liver was swollen and appeared mottled due to uniformly distributed pale spots which accentuated the lobular pattern. The thoracic and peritoneal cavities contained serous fluid and strands of fibrin. The microscopic lesions of the hearts of poisoned rabbits were characterized by fine vacuolation of myocardial fibers. The vacuoles were arranged in rows between myofibrils and around muscle nuclei and were the result of swelling of mitochondria and the accumulation of droplets of neutral fat. Swelling of mitochondria was accompanied by a change in the permeability of the mitochondrial membranes. Degeneration of cardiac muscle fibers followed the vacuolation and took 1 of 2 forms. The more common form, myofibrillar degeneration, appeared as a progressive disorganization of myofibrillar A-band patterns. The less common form was hyaline degeneration. An inflammatory reaction characterized by infiltration of small numbers of neutrophils and macrophages and hyperplasia of interstitial fibrocytes occurred in the areas of degeneration but regeneration of cardiac muscle fibers was rarely observed. Myocardial degeneration and congestive cardiac failure produced passive venous congestion of the liver and degeneration of hepatocytes consistent with hypoxic changes. Extensive degeneration of skeletal muscle was found in only 1 rabbit which had been given a large total dose of coffee senna. The response of skeletal muscle fibers of poisoned rabbits to a mild crushing injury was similar to the response of control rabbits. The predominant form of regenerative response to this injury in control and poisoned rabbits was discontinuous regeneration which was virtually complete in 10 days. Continuous regeneration was apparent for up to 30 days in areas of cicatrization or residual necrotic debris..