Showing papers on "Fibrinoid necrosis published in 1969"
TL;DR: There was a total occlusion of the artery supplying the territory of the infarct in 45 of 50 consecutive lacunes, and segmental arterial disorganization has been discussed in some detail.
Abstract: The arterial lesions causing lacunes have been investigated using serial sections of blocks of the basal ganglia and pons from four cases with a history of hypertension and small strokes. In 45 of 50 consecutive lacunes there was a total occlusion of the artery supplying the territory of the infarct. The associated vascular lesions were as follows: segmental arterial disorganization 40 (with enlargement 31, with hemorrhage 26, with fibrinoid deposit 14), thrombosis of a fusiform asymmetric microaneurysm, 2; plaque of foam cells (atherosclerosis) 3; complete absence of any lesion 1; suspected segmental disorganization 3; and miscellaneous 1. Segmental arterial disorganization has been discussed in some detail. Others have termed this condition hyalinosis, angionecrosis with aneurysm formation, plasmatic destruction, fibrinoid necrosis, fibrinoid arteritis, etc.
668 citations
TL;DR: Ischemic change was observed in the heart and brain as a result of the acute arteritis, and the pathologic changes were attributed to a severe vasculitis characterized by extensive fibrinoid necrosis and endothelial swelling.
Abstract: Gross and microscopic changes of the joint, heart, and brain were studied in chickens infected intravenously with M. gallisepticum (S6 isolate). Synovitis occurred within 3 days, followed by suppurative arthritis at 7 days, and osteomyelitis 5 days later. The pathologic changes were attributed to a severe vasculitis characterized by extensive fibrinoid necrosis and endothelial swelling. Ischemic change was observed in the heart and brain as a result of the acute arteritis.
11 citations
TL;DR: The pathogenesis of the hemolytic-uremic syndrome has not been established, and, indeed, all cases may not arise from the same pathogenetic mechanisms.
Abstract: The association of acute hemolytic anemia, thrombocytopenia and renal failure was described by Casser et al.1 in 1955. Since that time, several hundred cases have been reported, mainly in children. In adults, the hemolytic-uremic syndrome is often associated with pregnancy. The similarity to thrombotic thrombocytopenic purpura has suggested to some that the conditions may be related. The pathogenesis of the hemolytic-uremic syndrome has not been established, and, indeed, all cases may not arise from the same pathogenetic mechanisms. Renal lesions have included a severe glomerulitis (termed thrombotic microangiopathy), cortical necrosis and acute necrotizing glomerulonephritis. Fibrinoid necrosis and thrombosis of arteries . . .
3 citations
TL;DR: Parenteral administration of this substance caused fibrinoid lesions of the small cerebral arteries and arterioles probably due to the increased permeability of the vessel walls, as indicated by the histological changes of the damaged vessels.
Abstract: The nature of vascular toxic substance (necrotizing substance) in the extracts of clamped rabbit renal cortex was investigated. Analysis of the kidney tissue extracts by means of column chromatography, measurement of ultraviolet absorption, dialysis and heating test revealed that the substance was not renin, but rather a substance with lower molecular weight which was nondialyzable, heat-stable (not destroyed by heating for 10 min. at 100°C). Parenteral administration of this substance, without elevating blood pressure, caused fibrinoid lesions of the small cerebral arteries and arterioles probably due to the increased permeability of the vessel walls, as indicated by the histological changes of the damaged vessels.
3 citations
Journal Article•
2 citations
TL;DR: Based on the findings, the sudanophilia of the media has been attributed to lipids rendered visible by phanerosis.
1 citations