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At least 991 records · Page 55Linked to original sources
PubMed1995

Impaired biliary excretion and whole body elimination of methylmercury in rats with congenital defect in biliary glutathione excretion.

Biliary excretion of methylmercury, a major route of elimination of this toxic compound, was less than 2% of control in Eisai hyperbilirubinemic (EHBR) rats, a mutant Sprague-Dawley strain with a defect in biliary excretion of a variety of organic anions, including glutathione S-conjugates and reduced glutathione (GSH). Biliary GSH excretion in EHBR rats was also < 2% of controls, confirming previous findings. Impaired biliary methylmercury and GSH excretion was not explained by decreased hepatic content of these compounds. Indeed, hepatic methylmercury and GSH concentrations in EHBR rats were actually double those of controls. To assess the significance of the impaired biliary excretion in the whole body elimination of the toxicant, 203Hg excretion was measured over a 17-day period after intraperitoneal administration of either 0.5 or 5 mumol/kg of 203Hg-methylmercury chloride. The results for the two doses were similar. Methylmercury was eliminated by a first order process; however, the biological half-line was significantly longer in the EHBR rats, 46 to 54 days versus 18 to 22 days. Fecal excretion was the main route of elimination in both control and mutant animals. At necropsy (17 days), 16% to 25% of the 203Hg dose was recovered in the liver of the EHBR rats, whereas livers of control animals contained less than 2%of the administered dose. These findings demonstrate the biliary excretion of methylmercury is markedly impaired in EHBR rats and is associated with a low biliary GSH excretion, providing support for the hypothesis that methylmercury is normally transported across the canalicular membrane by a GSH-dependent mechanism, and presumably as a GSH mercaptide (CH3Hg-SG).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Pathology of congenital defects of the central nervous system vessels].

The author's classification of vascular malformations in the central nervous system is presented approved by neurosurgeons, pathologists and in forensic medicine. The description of the cavernous angiomas pathology is given showing possibility of their radical surgery. The notion of micro-malformation is formulated. The pathogenetic concept of Sturge-Weber disease with recommendations for the clinics is given. The author's model of the malformation morphogenesis in the vessels of the central nervous system is presented and the ways for the decrease in the incidence of these malformations are indicated.

Brain↗
PubMed1995

[A case report on a reconstructive operation of a traumatic tricuspid regurgitation with a congenital defect of the left pericardium].

We reported a successful tricuspid valve replacement in a 58-years old man, who had easy fatiguability after 14 years of a blunt chest trauma. The preoperative examination revealed a marked cardiomegaly with deformation of both ventricles and grade 4 tricuspid regurgitation caused by the prolapse of the anterior leaflet. The operative inspection revealed a left pericardial defect with a diameter of 10 cm and a torn anterior papillary muscle. Since a usual plastic procedure did not improve the regurgitation, a Carpentier-Edward bioprosthetic valve was implanted in the supra annular position. Atrioventricular conduction was preserved. The tricuspid valve was not resected to preserve the ventricular function. The patient recovered his own activity.

Heart Injuries↗