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

Abstract

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 micrograms 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.

Terbufos-sulfone exacerbates cardiac lesions in diabetic rats: a sub-acute toxicity study

“…Ultrastructural changes after acute OPC poisoning have been reported by numerous clinical case studies (31)(32)(33)(34). We also observed similar cardiac lesions in diabetic rats with sub-acute and apparently non-lethal exposure to TS.…”

Involvement of cardiomyocyte apoptosis in myocardial injury of hereditary epileptic rats

“…Since then, a wide range of cardiac arrhythmias have been reported, ranging from atrial fibrillation, supraventricular tachycardia, prolonged QT intervals, and torsades de pointes (Nilsson et al 1997;Nei et al 2004;Schuele 2009;Sevcencu and Struijk 2010). Also, a number of studies have indicated that seizure activity produces cardiac dysfunction and myocardial damage in human patients (Legriel et al 2008;Shimizu et al 2008) as well as animals experiencing seizures that were induced by lethal nerve agents (Tryphonas et al 1996). Several studies have shown that seizures could result in myocardial injury by a variety of mechanisms.…”

Nasal midazolam as a novel anticonvulsive treatment against organophosphate-induced seizure activity in the guinea pig

“…It is well established that EGSA, which accompanies exposure to OP agents, contributes to the profound brain damage and cardiac pathology observed after intoxication with OP compounds (Lemercier et al 1983;Shih 1993, 1997;Mcleod 1985;Mcleod et al 1984;Petras 1981;Philippens et al 1981;Singer et al 1987;Tryphonas and Clement 1995;Tryphonas et al 1996). These findings emphasize the importance of identifying possible pharmacological interventions that will minimize the damage induced by the OP intoxication.…”

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