HISTOMORPHOGENESIS OF SOMAN-INDUCED ENCEPHALOCARDIOMYOPATHY IN SPRAGUE-DAWLEY RATS

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Authors
  1. Tryphonas, L.
  2. Clement, J.G.
Corporate Authors
Defence Research Establishment Suffield, Ralston ALTA (CAN)
Abstract
Although myocardial damage caused by soman has been previously reported, its relation to brain damage is unclear. In order to clarify this relationship, we examined the histomorphogenesis of central nervous system (CNS) and myocardial lesions in Sprague-Dawley rats, given atropine methylnitrate (20 mg/kg) and HI-6 (125 mg/kg) ip 10 min before a single injection of 0 or 130 mu g soman/kg (sc) and sacrificed 45 min and 1.5 hr, 3 hr, 24 hr, and 72 hr later. Bilaterally symmetrical CNS damage began with vacuolation of the neuropil and was followed by astrocytic degeneration and neuronal necrosis culminating in liquefaction necrosis and focal hemorrhage. The cerebral cortex, limbic system, thalamus, and substantia nigra were common target sites. Repair in affected sites was characterized by capillary endothelial cell proliferation, microgliosis, and reversal of microvacuolation. Myocardial damage began with myocytolysis and contraction bands and evolved into coagulative myocytolysis and replacement fibrosis with a transient recruitment of acute inflammatory cells. The left ventricle, especially its free wall and papillary muscules, was consistently affected. There was good correlation among seizures, CNS damage, and myocardinal lesions at all times following treatment. The results support the view that CNS lesions are associated with protracted seizure activity and provide evidence that myocardial damage is neurogenic.
Keywords
Brain hemorrhage;Encephalocardiomyopathy;Myocardial fibrosis;Myocytolysis
Date of publication
01 Nov 1995
Number of Pages
17
Reprinted from
Society of Toxicologic Phatologists, vol 23, no 3, 1995, p 393-409
DSTKIM No
96-01938
CANDIS No
180693
Format(s):
Document Image stored on Optical Disk;Hardcopy

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