Premium
Causality of parenchymal and vascular changes in rats with experimental thiamine deficiency encephalopathy
Author(s) -
Chen Qi,
Okada Shinobu,
Okeda Riki
Publication year - 1997
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.1997.tb04452.x
Subject(s) - thiamine , pathology , parenchyma , encephalopathy , medicine , thiamine deficiency , causality (physics) , wernicke's encephalopathy , physics , quantum mechanics
The causality of vascular and parenchymal damage to the central nervous system (CNS) was examined In rats with thiamine deficiency. Male Sprague Dawley rats were divided Into two groups; one was given a thiamlne‐deficient diet ODD) and Injected Intraperitoneally with 10μg/100g bodyweight pyrithlamine (PT) In order to analyze morpho‐metrically the topographical and sequential relationship between vascular and parenchymal changes and vase dilatation, and the other was given a TDD and 50 μg/100 g bodyweight PT in order to determine hemorrhagic sites using serial dons. Histological examination showed that sponglotic change occurred selectively in the Interior colllculus (100%) from day 19, and thereafter In the thalamus (95%), mammlllary body (50%) and nuclei olivaris and vestlbularls of the pons (25%), with or without hemorrhage. Simultaneously, glycogen accumulation was also observed In these regions at a frequency similar to that of hemorrhage. Ultrastructurally, however, hydroplc swelling of astrocytic and neuronal processes without glycogen accumulation was observed as early as day 9 In the inferior cofliculus, at which time an Increase of glial fibrillary acldic protein‐positive processes was also recognized. The Superior colllculus was completely spared. From day 22 vasodilatation of the Inferior colliculus occurred, concomltantly with bodyweight loss and neurological symptoms. Twenty‐two examined hemorrhages, which occurred in the thalamus and Inferior colliculus, were distributed along the arterioles or capillarles on the arterial side. In conclusion, the morphological CNS changes caused by thiamine deficiency with administration of low‐dose PT in rats begin as hydropic swelling of neuronal and astrocytic processes, followed by hemorrhage and, thereafter, by vasodllatatlon. The predilectlon for hemorrhage on the arterial side without parenchymal changes suggests that petechial hemorrhage Is not simply secondary to parenchymal changes, but Is due to hemadynamlc change resulting from thlamfne deficiency‐Induced vascular dysfunction.