Hemorrhage of Thiamine-deficient Encephalopathy
- 1 September 1981
- journal article
- research article
- Published by Oxford University Press (OUP) in Journal of Neuropathology and Experimental Neurology
- Vol. 40 (5) , 566-580
- https://doi.org/10.1097/00005072-198109000-00007
Abstract
Hemorrhagic lesions of pyrithiamine-induced acute thiamine-deficient encephalopathy of the mouse (PIATDEM) consisted of petechiae, which often coalesced to form small hematomas. Electron microscopy showed the typical petechial lesion to be composed of a perivascular necrotic zone containing fibrin-platelet clot surrounded by a ring of erythrocytes. Endothelial cells were intact and tight junctions were closed. A study of permeability to horseradish peroxidase (HRP) revealed only a slight increase in the number of transport vesicles in the endothelial cells. A large amount of HRP present in the lesions seemed to have entered the brain by a hemorrhagic route which remains unclarified. Spherical latex particles, 0.23 µm in diameter, were injected intravenously into encephalopathic mice at a time when intracerebral hemorrhages frequently occurred. Two to 24 hours after the injection, a large number of latex particles penetrated the blood vessels at sites of hemorrhage. There were many particles in the phagosomes of the endothelial cells, which suggested transendothelial transport by the organelle. The possibility of endothelial phagocytic transport of erythrocytes as a main route of diapedesis is discussed.This publication has 11 references indexed in Scilit:
- New ultrastructural evidence for a protein transport system in endothelial cells of gerbil brainsActa Neuropathologica, 1979
- Pyrithiamine-induced acute thiamine-deficient encephalopathy in the mouseExperimental and Molecular Pathology, 1978
- HEMORRHAGIC TOXINS FROM RATTLESNAKE (CROTALUS-ATROX) VENOM - PATHOGENESIS OF HEMORRHAGE INDUCED BY 3 PURIFIED TOXINS1978
- MARROW CELL EGRESS - SPECIFICITY OF SITE OF PENETRATION INTO SINUS1978
- TRANSENDOTHELIAL VESICULAR TRANSPORT OF PROTEIN FOLLOWING COMPRESSION INJURY TO SPINAL-CORD1976
- CAPILLARY HEMORRHAGE IN ASCORBIC-ACID-DEFICIENT GUINEA PIGS - ULTRASTRUCTURAL BASIS1968
- The Mechanism of Thrombocytopenic BleedingAmerican Journal of Clinical Pathology, 1966
- PLATELET PHAGOCYTOSIS AND AGGREGATIONThe Journal of cell biology, 1965
- THE SITE OF LEUCOCYTE EMIGRATION DURING INFLAMMATIONQuarterly Journal of Experimental Physiology and Cognate Medical Sciences, 1961
- Wernicke's disease - Identity of lesions produced experimentally by B1 avitaminosis in pigeons with hemorrhagic polioencephalitis occurring in chronic alcoholism in man1940