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Toxicologic Pathology
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Journal Article

Early Histopathologic and Ultrastructural Changes in the Heart of Sprague-Dawley Rats Following Administration of Soman

Leander Tryphonas

Department of Pathology and Laboratory Medicine, Faculty of Medicine, University of Ottawa, Ontario, Canada K1H 8M5

John P. Veinot

Division of Laboratory Medicine, Ottawa Civic Hospital, Ottawa, Ontario, Canada K1Y 4E9

John G. Clement

Medical Countermeasures Section, Defence Research Establishment Suffield, Ralston, Alberta, Canada TIA 8K6

Male Sprague-Dawley rats were given atropine methylnitrate (20 mg/kg) and HI-6 (125 mg/kg) ip 10 min before a single injection of 130 µg soman/kg sc, and the heart was examined by light and electron microscopy 10, 25, 45, 90, and 180 min after the onset of seizures. Seizures appeared within 6-11 min after treatment. Control rats were given saline sc in place of soman. Early myocardial lesions consisting of hypercontraction and hyperextension of sarcomeres, focal myocytolysis, and contraction bands were detected in individual or groups of myocardial fibers. Hypercontraction was characterized by shortening of the sarcomere length, disappearance of the I and H bands, and thickening of the Z line. In contrast, hyperextended sarcomeres had thickened I and H bands. Myocytolysis was characterized by a progressively severe focal dissolution of myofilaments and edema of the affected sarcoplasmic area. Contraction bands appeared to result from the breakdown of markedly hypercontracted myofibril bundles. Due to the presence of a number of surviving myofilaments and the preservation of the sarcolemmal tube, distortion of the overall myocytic structure was minimal. Changes in the mitochondria and other intracellular organelles were also minimal and nonspecific. The close resemblance of morphologic findings to those induced by catecholamines supports the view that soman-induced myocardial damage is secondary to a treatment-related release of unphysiologic amounts of endogenous catecholamines.

Key Words: Catecholamines • cholinesterase inhibitors • encephalocardiomyopathy • hypercontraction • hyperextension • myocytolysis • toxic cardiomyopathy

Toxicologic Pathology, Vol. 24, No. 2, 190-198 (1996)
DOI: 10.1177/019262339602400207
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