[Disseminated intravascular coagulation: a clinical study].
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Biomedical subjects
Publications and source records attributed to N Robinson.
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Electrodes were implanted into the rat hippocampus in both hemispheres for increasing periods of up to 60 days, and the effects of trauma and electrical stimulation of enzymes controlling cell metabolism in the region of implantation were examined and assessed in relation to studies on humans. In the unstimulated hippocampus as a control, enzyme changes were mainly confined to a narrow area of tissue damage surrounding the electrode. The enzyme changes in response to trauma varied widely; some enzymes controlling tissue respiration showed early and rapid changes, increasing in hyperactive, swollen glial cells and vascular endothelium and decreasing in nerve cells and neuropile. Acid phosphatase activity also increased rapidly in glial cells; other phosphate-releasing enzymes increased more gradually with time. A turning point in these chages was apparent between 25 and 40 days, followed by a reversion to more normal levels at 60 days. Electrical stimulation of the hippocampus in the contralateral hemisphere produced no detectable enzyme changes from those of the unstimulated hippocampus.
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The enzyme response to injury of the brain was well localized and limited. Some enzymes, even in 12 day old brain, increased rapidly, mainly in neocortical glial cells. In the corpus callosum enzymes were not significantly hyperactive before the light myelination stage. Some hyperactivity declined after 21 days. Oxidative processes and phosphate metabolism were most disturbed.
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Penetration of a microneedle and injection of 4 μl. saline into the neocortex of the 5 day old rat brain produced no changes in behaviour of the rats up to 21 days post-injection. Within 24 hours sections indicated that tissue damage was apparent only at the pia-arachnoid membrane and where fluid was released; elsewhere the needle pathway was identified by the enzyme response. The enzyme histochemistry showed a marked increase in glial cell activity of some phosphatases within 24 hours at the site of injury; the pia-arachnoid and outer limiting membrane also showed abnormally high phosphatase reactions. NADH(2)-diaphorase was the only dehydrogenase that was raised in some nerve and glial cells at 24 hours post-injection but other dehydrogenases, mainly LDH and SDH, showed changes at four days post-injection. The phosphatases and 5'-nucleotidase previously showing intense glial cell enzyme reactions appeared to reach peaks of activity at eight days, and at 16 days the onset of scarring was apparent. In the pia-arachnoid enzyme activity increased to 21 days. Some enzymes, particularly AChE and MAO, showed no alterations of note throughout.
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