EARLY HISTOPATHOLOGIC AND ULTRASTRUCTURAL-CHANGES IN THE HEART OF SPRAGUE-DAWLEY RATS FOLLOWING ADMINISTRATION OF SOMAN

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 mu g s oman/kg sc, and the heart was examined by light and electron microscop y 10, 25, 45, 90, and 180 min after the onset of seizures. Seizures ap peared within 6-11 min after treatment. Control rats were given saline sc in place of soman. Early myocardial lesions consisting of hypercon traction and hyperextension of sarcomeres, focal myocytolysis, and con traction bands were detected in individual or groups of myocardial fib ers. Hypercontraction was characterized by shortening of the sarcomere length, disappearance of the I and H bands, and thickening of the Z l ine. In contrast, hyperextended sarcomeres had thickened I and H bands . Myocytolysis was characterized by a progressively severe focal disso lution of myofilaments and edema of the affected sarcoplasmic area. Co ntraction bands appeared to result from the breakdown of markedly hype rcontracted myofibril bundles. Due to the presence of a number of surv iving myofilaments and the preservation of the sarcolemmal tube, disto rtion of the overall myocytic structure was minimal. Changes in the mi tochondria and other intracellular organelles were also minimal and no nspecific. The close resemblance of morphologic findings to those indu ced by catecholamines supports the view that soman-induced myocardial damage is secondary to a treatment-related release of unphysiologic am ounts of endogenous catecholamines.