A case of spontaneous myocardial necrosis and cerebral ischemic lesions in a laboratory beagle dog

Abstract

A beagle dog treated with saline as a control animal in a preclinical study was euthanized due to sudden systemic deterioration. On histopathological examination, contraction band necrosis of myocardial cells was observed widely in the left ventricular wall, including the papillary muscle and apex, and observed slightly in the ventricular septum and left atrium. In the brain, necrosis was observed in neurons and glia of the cerebral cortex, hippocampal pyramidal cells, glial cells of the rostral commissure and Purkinje cells of the cerebellar vermis. It is highly probable that the marked systemic deterioration was caused by cardiac dysfunction due to the spontaneous contraction band necrosis of the myocardial cells, although the pathogenesis of the myocardial lesions remains unclear. Given the distribution of neuronal necrosis in the brain, it is likely that these lesions resulted from the ischemia responsible for acute cardiac failure.

Keywords: beagle dog; contraction band necrosis; ischemic brain lesion; spontaneous lesion.

Fig. 1.

Histopathological features of the dog’s heart. Transverse hypercontraction bands spanning myofibers were extensive in the left ventricle (a). Slight hemorrhage (b) and neutrophil infiltration (c) accompanied contraction band necrosis. Hematoxylin and eosin staining.

Fig. 2.

Histopathological features of the dog’s brain. Necrosis of neurons and glia was observed in the piriform lobe of the cerebral cortex accompanied by a vacuolated neuropil (a). Necrosis of hippocampal pyramidal cells (b), glial cells with nuclear pyknosis in the rostral commissure (c) and Purkinje cells in the cerebellar vermis (d) was observed. Arrows and arrowheads demarcate necrotic glial cells and Purkinje cells, respectively. Neither gliosis nor microglial reactions were observed in these brain lesions. Hematoxylin and eosin staining.