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J V Lafuente

Publications and source records attributed to J V Lafuente.

6 recordsLinked to original sources
PubMed1992

Ultraviolet irradiation induced brain oedema in rats. A microgravimetric study.

The cerebral cortex of 36 anaesthetized Wistar rats were exposed to ultraviolet irradiation (UV-I) for 6 min through a 2 x 2 mm left parietal craniotomy. Animals were killed at different times and brains were removed immediately after death. Three consecutive coronal sections were obtained and sampled for gravimetric study. The density of the samples was measured using a continuous gradient of organic solvents. Gravimetric results showed significant differences between brain samples. The irradiated left hemisphere was less dense than the right one, and maximum differences in density were found in the medial coronal section. Grey and white matter oedema in the non-irradiated hemisphere was compared with the irradiated hemisphere. Early and delayed onset of odema was observed in both hemispheres but it was more marked in the irradiated hemisphere. In conclusion, brain oedema induced by ultraviolet irradiation in various animals is also reproducible in rats with all the advantages involved in the use of these experimental animals. Microgravimetric study correlated with topographical analysis using this model may lead to an understanding of some of the dynamic aspects of cerebral oedema.

Animals↗
PubMed1991

Traumatic brain injuries: structural changes.

A host of complications and consequences may follow a contusion or other brain injury of any sort. An appreciation of the temporal evolution of the contusion from a microscopic standpoint is useful to a full understanding of the process by which physical force damages the brain and how the brain reacts to this damage. Some disruptions of the blood brain barrier quite early will result in extracellular edema. The microscopic appearance of an edematous area is usually spongy with numerous vacuoles. The neuropil may appear bubbly, and glial cells may be swollen. If edema has been long standing, the vacuoles may be larger and in fact a small cyst may appear in the white matter. If focal cerebral edema is not present for long periods of time and the underlying cause has been corrected, residual fluid and electrolytes are eventually removed, restoring the neuropil to a normal state, leaving no sign of its presence. However, in longer standing lesions, myelin pallor and some reactive gliosis may remain indefinitely. Neurons may show swelling very early and for a short period of time, which gives way to shrinkage, eosinophilia, and nuclear pyknosis. These changes may be observed at the periphery of lesions for as long as 5 or 6 months after the initial event. Before dissolution, nuclear pyknosis may remain in the tissue for many days and possibly longer, and may even become mineralized in situ (ferruginated neurons) to remain for years. In a traumatic lesion, swollen and ballooned axons may be found in and around the contusion but also at great distances from it (diffuse axonal injury). Axonal ballooning may be observed between 24 and 48 h postinjury and may persist wherever found for many years. Selective axonal calcification has been observed in humans as well as in experimental trauma. At about 7-10 days postinjury increased numbers of astroglia probably are present. Over the ensuing weeks and months, and probably years, astrocytes increase in number and in fibrillary appearance, eventually resulting in a glial scar in and about the injured area. It is thought that this reactive gliosis results in restoration of the blood-brain barrier in the damaged area.

Astrocytes↗
PubMed1990

Dynamics of tracer distribution in radiation induced brain oedema in rats.

The dynamic behaviour of the distribution of Evans blue (EB), sodium fluorescein (SF), Lucifer yellow (LY) and horseradish peroxidase (HRP) was studied using standard light- and fluorescence microscopy following ultraviolet radiation induced brain oedema in the rat model. The cerebral cortex was irradiated after craniotomy (2 x 2 mm) under anaesthesia. The tracers were injected (iv) 30 min prior to radiation. Animals were perfused with glutaraldehyde through the heart at different survival periods ranging from 30 min to 24 h post irradiation. The results showed a remarkable difference in distribution and spread of these tracers in the oedematous brain following radiation. The extravasation of EB was evident in ipsilateral cortex 6 h after radiation which extended to the contralateral side at the end of the 24 h survival period. The HRP reaction product was seen in the necrotic area 3 h after radiation which further extended to the underlying white matter at 24 h survival. The LY stained the ipsilateral micronecrotic area 6 h after radiation, whereas a non-specific diffuse fluorescence of SF was noted at this time period. These results point out a specific selectivity of tracer distribution in oedematous brain following ultraviolet radiation.

Animals↗
PubMed1989

Pelizaeus-Merzbacher disease with thiamine deficiency or Leigh disease with extensive involvement of white matter? Case report.

We report on a case of a 30-month-old child who presented with a clinical syndrome compatible with leucodystrophy and in whom neuropathological features of both Pelizaeus-Merzbacher disease and subacute necrotizing encephalopathy were shown. The significance of the neuropathological findings is discussed in the light of a possible coexistence of both diseases which has not previously been reported.

Brain↗