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  • 1
    ISSN: 1432-0533
    Keywords: Key words Hypothermia ; Spinal cord trauma ; Albumin ; Fibrinogen ; Fibronectin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Systemic hypothermia has neuroprotective effects in experimental models of central nervous system ischemia caused by vascular occlusions. The present study addresses the question as to whether systemic hypothermia can influence the extravasation of plasma proteins following severe spinal cord compression trauma using immunohistochemistry to identify the plasma proteins albumin, fibrinogen and fibronectin. Fifteen rats were assigned to one of three groups and received either thoracic (T) laminectomy or severe spinal cord compression trauma of the T8–9 segment. One group comprised laminectomized animals without compression trauma submitted to a hypothermic procedure in which the core temperature was reduced from 38° to 30 °C. The two trauma groups were either submitted to the same hypothermic procedure or kept normothermic during the corresponding time. All animals were killed 24 h following the surgical procedure. The normothermic and hypothermic trauma groups had indications of marked extravasation of albumin, fibrinogen and fibronectin at the site of the injury (T8–9). There was also pronounced extravasation in the cranial and caudal peri-injury zones (T7 and T10) of normothermic injured rats but, with few exceptions, not in the hypothermic ones with the same degree of compression. By measuring the cross-sectional area of the peri-injury zones we found in the hypothermic trauma group a significant reduction of the expansion compared with that present in normothermic injured rats. Our study thus indicates that hypothermia reduces the extravasation of the plasma proteins albumin, fibrinogen and fibronectin following spinal cord compression in the rat. Such a reduction may contribute to neuroprotective effects exerted by hypothermia.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 25 (1973), S. 149-160 
    ISSN: 1432-0533
    Keywords: Nutritional Encephalopathy ; Brain Edema ; Vitamin E Deficiency ; Electron Microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Focal lesions were induced in the cerebellum by feeding chickens a diet high in unsaturated fats and deficient in vitamin E. Ultrastructurally, the lesions consisted of central and peripheral zones. The central zone was characterized in the cortex and white matter by enlargement of the intercellular space, swelling of astrocytes, vacuolization of oligodendrocytes, ballooning of nerve fibers, degenerative changes in small blood vessels, and extravasation of plasma and blood cells. The peripheral zone was characterized by enlargement of the intercellular space in the white matter, swelling of astrocytes in the cortex, and the accumulation of dark bodies in the endothelium of small blood vessels. The results suggest that this nutritional encephalopathy is caused by alterations in the permeability of the vascular bed due to the dietary stress of unsaturated fatty acids in the absence of vitamin E.
    Type of Medium: Electronic Resource
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