Histochemical and electron microscopic studies of acute cardiomyopathy induced by restraint stress in pigs.
In 23 healthy crossbred pigs of Yorkshire and Swedish Landrace (body weight 85 to 90 kg), stress was produced by pharmacological restraint. Cardiac lesions were observed in all the experimental animals, but no alterations were seen in the 9 controls. The lesions consisted of focal myocardial necrosis with infiltration of mononuclear inflammatory cells. Histochemical stains for two dehydrogenases, cytochrome oxidase and unspecific esterase, were applied to fresh-frozen sections of heart muscle. The damaged muscle fibers exhibited initially an increase in formazan deposits, and then a decrease and total loss of enzymatic activity. A reduction or total loss of glycogen and accumulation of lipids were demonstrated in the damaged myocardium ultrastructurally. The mitochondria were swollen with focal loss of the cristae. They often exhibited electron-dense of diverse appearance. In degenerating cells, the myofilaments usually lacked the normal cross-striations whereas, in necrotic foci, the changes ranged from clumping to complete lysis of the myofilaments. The sarcoplasmic reticulum and the T system contained numerous dilated vesicles in cells with mitochondrial and myofibrillar damage. It was concluded that the myocardial alterations, following restraint stress, were caused by a reflex liberation of cardiotoxic catecholamines.
D000818:Animals; D008058:Dihydrolipoamide Dehydrogenase / Q000378:metabolism; D005260:Female; D006003:Glycogen / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000473:pathology*; D009210:Myofibrils / Q000473:pathology; D009336:Necrosis; D013312:Stress, Physiological / Q000473:pathology*; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013552:Swine
D006003:Glycogen; D007770:L-Lactate Dehydrogenase; D013385:Succinate Dehydrogenase; D008058:Dihydrolipoamide Dehydrogenase