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Biomedical subjects

J W Finnie

Publications and source records attributed to J W Finnie.

At least 55 records · Page 3Linked to original sources
PubMed1990

Effect of tunicamycin on the blood-brain barrier and on endothelial cells in vitro.

In guinea-pigs given 400 micrograms per kg of tunicamycin, the toxin responsible for the disease known as annual ryegrass toxicity, alterations in blood-brain barrier permeability were assessed with vascular tracers of differing particle size. The toxin caused loss of integrity of the barrier to the smallest diameter tracer, horseradish peroxidase, but the cerebral endothelium was able to retain larger particles of ferritin and colloidal gold in the circulation. The effect of tunicamycin on cultured endothelial cells was characterized by dose-dependent lethal damage to these cells, marked dilatation of cisternae of RER, severe cytoplasmic vacuolation and a reduced incidence of mitosis in surviving endothelial cells. It was concluded that tunicamycin is able to damage directly endothelial cells, with a resultant increase in cerebral vascular permeability.

Animals↗
PubMed1989

Acute hepatotoxicity with resultant pulmonary and cerebral embolism in guinea pigs given tunicamycin.

The hepatotoxicity of tunicamycin was studied in 8 to 10-week-old guinea pigs. Acute hepatic damage was produced consistently in guinea pigs given a single dose of 400 micrograms/kg of tunicamycin and observed at intervals up to 72 h post-injection. Significant elevations occurred in serum levels of liver enzymes and ammonia, while concentrations of serum proteins were lowered. A periportal pattern of hepatocellular damage, with death of many hepatocytes, was consistently observed by 72 h. Severe vacuolation of hepatocytes resulted from lipid accumulation and dilatation of cisternae of rough endoplasmic reticulum, and bile ductule hyperplasia was also observed. Swollen hepatocyte cytoplasm protruded into many hepatic blood vessels, and detached portions of hepatocytes produced emboli in pulmonary and cerebral capillaries, thus contributing to capillary occlusion in the brains of treated guinea pigs.

Animals↗
PubMed1988

Pathological and pathogenetic changes in the central nervous system of guinea pigs given tunicamycin.

Guinea pigs were injected with tunicamycin and the sequential morphological alterations in the brain examined to investigate further the pathogenesis of cerebral lesions in this experimental model of annual ryegrass toxicity, a central nervous system disease of livestock caused by members of the tunicamycin group of antibiotics. Brain damage was most commonly observed in the cerebellum, and the important alterations in the development of degenerative parenchymal lesions appeared to be largely referrable to changes in small blood vessels. Endothelial damage, with increased vascular permeability, resulted in capillary obstruction leading to localised ischaemia and hypoxic neuronal damage. There was evidence for several possible mechanisms which may have contributed to vascular occlusion.

Animals↗
PubMed1987

Focal spongy changes in the central nervous system of sheep and cattle.

A focal form of vacuolation in the white matter of the thalamus of 13 sheep and 2 cattle is described. The individual vacuoles were similar in appearance to those reported in other forms of spongy degeneration, but they were differentiated by their consistent neuroanatomical localization in the thalamic radiation of all 15 animals. Thirteen of these were sheep used in toxicity experiments and 11 had shown signs of convulsive activity.

Acetates↗
PubMed1986

Ultrastructural changes in the cerebellum of nursling rats given corynetoxin, the aetiological agent of annual ryegrass toxicity.

Nursling rats were given a lethal dose of corynetoxin and the sequential morphological alterations in the cerebellum were examined at daily intervals up to 3 days post-inoculation. Ultrastructural changes were those of cerebral vascular damage, which was usually focal in affected endothelial cells, and resulted in vascular stasis or thrombosis. These changes ultimately constituted a failure of perfusion in focal areas of brain parenchyma supplied by these vessels, resulting in necrosis.

Animals↗
PubMed1984

Histopathological changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

The distribution, severity and frequency of brain lesions produced in mice by the administration of Clostridium perfringens Type D epsilon toxin were examined by light microscopy. The granular layer of the cerebellum was the area most frequently affected in mice given single doses of toxin. Sequential changes in brain morphology were examined from 1 h to 7 days after injection of toxin. Lesions progressed from an initial vasogenic oedema to malacic foci which commonly were focal and bilaterally symmetrical, with a predilection for white matter. The topographical distribution of these malacic areas is discussed.

Animals↗
PubMed1984

Ultrastructural changes in the brain of mice given Clostridium perfringens type D epsilon toxin.

Mice were given lethal and sublethal doses of Clostridium perfringens Type D epsilon toxin and the early morphological changes in perfusion-fixed intoxicated brains were examined from 30 min to 6 h post-inoculation. The initial ultrastructural finding was swelling of astrocytes, especially the perivascular extensions of these cells. Astrocytes in the cerebellum appeared to be particularly sensitive to this toxin. These changes were quickly followed by evidence of severe endothelial damage, with the endothelial cytoplasm becoming attenuated, vacuolated and very electron-dense. A pathogenetic sequence of events leading to malacia, derived from ultrastructural observations, is proposed.

Animals↗