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L Tryphonas

Publications and source records attributed to L Tryphonas.

43 records · Page 3Linked to original sources
PubMed1970

The pathology of arylmercurial poisoning in swine.

To produce arylmercurial poisoning, phenylmercuric chloride (PMC) was administered daily to 30 healthy five week-old piglets for periods of up to 90 days. The dosage used ranged from 0.19 to 4.56 mg of mercury (Hg)/kg. Levels exceeding 2.28 mg Hg/kg daily were moderately toxic. The disease occurring in this intoxication resulted from injury to the kidneys and large intestine. Fetid diarrhea and failure to gain weight were consistent clinical signs. The primary gross lesions were necrotic typhlitis and colitis, and nephrosis. Degeneration and necrosis were found in affected organs. Regeneration was prominent in the proximal convoluted tubules. The pathology of this disease was similar to that described for mercuric chloride poisoning in other species and, presumably, reflected the ease with which PMC was metabolized to release mercuric ion.Tissue analysis for mercury suggested that only certain target organs, such as kidney and colon, accumulated significantly high levels of mercury. This, presumably, resulted from rapid metabolism of the compound and excretion of mercuric ion in the kidney and colon. The net effect was to spare other tissues, and to injure the excretory organs when the dose level was sufficiently high.

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PubMedDate not supplied

Histomorphogenesis of soman-induced encephalocardiomyopathy in Sprague-Dawley rats.

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 micrograms 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 muscles, was consistently affected. There was good correlation among seizures, CNS damage, and myocardial 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.

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PubMedDate not supplied

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 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.

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