acid-phosphatase and Brain-Injuries

Morphologic changes and quantitative determination by enzymohistochemistry were studied during various survival times after cortical injury in 60 rats. It was found that acid phosphatase (ACP) showed regular changes with various survival times after cortical injury. The ACP content decreased from 30 min to 6 h, and began to increase after 6 h; the ACP content in the region around injury decreased over the period of 5 days to 3 weeks after; the ACP content in the injured region (region around injury and control region of injury) decreased in a linear fashion with the time. The linear correlation was very marked; one may accurately estimate the survival time with injury by the regression equation given.

Topics: Acid Phosphatase; Animals; Brain Injuries; Cerebral Cortex; Immunohistochemistry; Rats; Rats, Wistar

An investigation designed to define relationships between endothelial channels and lysosomes was conducted in the mammalian brain microvasculature. Microvessels from normal and mechanically injured mouse brains were studied ultracytochemically for: (1) transport of horseradish peroxidase (HRP) protein tracer through endothelial channels, and (2) for acid phosphatase (AcP) activity as an enzymatic marker of lysosomes. Following traumatic brain injury for 1 week with 2 h circulation of intravenously injected HRP, selected brain slices were processed for ultrastructural localization of either HRP, AcP, or for both reactions together within the same tissue slices. One week after blood-brain barrier (BBB) damage, the presence of HRP reaction product (RP) was observed within endothelial channels and vesicles of capillaries and arterioles with concomitant increase in lysosomal enzymatic activity of the endothelial cells bordering regions of brain damage. Lysosomes were observed to be directly connected to the endothelial channels. Our observations present cytochemical evidence for endothelial channel-lysosome connections which may suggest intralysosomal modification of blood-born materials before entering the neuropil. Such modification could have important immunological and/or metabolic significance.

Topics: Acid Phosphatase; Animals; Blood-Brain Barrier; Brain; Brain Injuries; Capillaries; Endothelium; Female; Horseradish Peroxidase; Lysosomes; Male; Mice; Microscopy, Electron; Time Factors

Topics: Acid Phosphatase; Animals; Brain Injuries; Brain Neoplasms; Enzyme Activation; Glucuronidase; Humans; Lysosomes; Neoplasms, Experimental; Rats

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Bony Callus; Brain Injuries; Child; Connective Tissue; Fracture Fixation, Internal; Fractures, Bone; Histocytochemistry; Humans; L-Lactate Dehydrogenase

This study demonstrates the changes of concentration and elimination of calcium, phosphate and zinc, as well as alteration of serum alkaline phosphatase and acid phosphatase especially in patients with severe brain injuries in connection with bone fractures. Because the study has not been completed, the presently acquired results should only demonstrate possible development of the examined parameters. To find out the pathogenesis of overgrowing callus in brain-injured patients, further examinations are being carried out to find the histochemical activities of alkaline and acid phosphatase, lactate dehydrogenase, adenosine triphosphatase and acetylcholine esterase.

Topics: Acid Phosphatase; Alkaline Phosphatase; Brain Injuries; Calcium; Humans; Phosphates; Skull Fractures; Wound Healing; Zinc

Topics: Acid Phosphatase; Animals; Brain Injuries; Female; Glucuronidase; Lysosomes; Male; Rats

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.

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Brain Injuries; Dihydrolipoamide Dehydrogenase; Electric Stimulation; Electrodes, Implanted; Glucosephosphate Dehydrogenase; Glycerolphosphate Dehydrogenase; Hippocampus; L-Lactate Dehydrogenase; Male; Monoamine Oxidase; NAD; Nucleotidases; Rats; Stereotaxic Techniques; Time Factors

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.

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Animals; Animals, Newborn; Brain; Brain Injuries; Cerebral Cortex; Corpus Callosum; Dihydrolipoamide Dehydrogenase; Esterases; Glucosephosphate Dehydrogenase; Glycerolphosphate Dehydrogenase; Histocytochemistry; L-Lactate Dehydrogenase; Monoamine Oxidase; Myelin Sheath; Nucleotidases; Oxidoreductases; Phosphoric Monoester Hydrolases; Pyrophosphatases; Rats; Succinate Dehydrogenase

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.

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Animals; Animals, Newborn; Arachnoid; Brain Injuries; Cerebral Cortex; Dihydrolipoamide Dehydrogenase; Glucosephosphate Dehydrogenase; Glycerolphosphate Dehydrogenase; L-Lactate Dehydrogenase; Magnesium; Monoamine Oxidase; NADH, NADPH Oxidoreductases; Nucleotidases; Oxidoreductases; Phosphoric Monoester Hydrolases; Pia Mater; Pyrophosphatases; Rats; Sodium Chloride; Succinate Dehydrogenase; Thiamine; Time Factors

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Brain; Brain Edema; Brain Injuries; Cold Temperature; Dexamethasone; Endopeptidases; Lysosomes; Rats

Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Animals; Brain; Brain Injuries; Cerebral Cortex; Corpus Callosum; Dihydrolipoamide Dehydrogenase; Enzymes; Glucosephosphate Dehydrogenase; Glycerolphosphate Dehydrogenase; Injections, Spinal; Male; Monoamine Oxidase; Nucleotidases; Pyrophosphatases; Rats; Succinate Dehydrogenase

Topics: Acid Phosphatase; Alkaline Phosphatase; Amidohydrolases; Animals; Brain Edema; Brain Injuries; Cathepsins; Cold Temperature; Glucuronidase; Histocytochemistry; Lysosomes; Mitochondria; Nerve Endings; Peptide Hydrolases; Phosphoric Monoester Hydrolases; Rats

Topics: Acid Phosphatase; Animals; Autoradiography; Brain Injuries; Central Nervous System; Histocytochemistry; Mitosis; Neuroglia; Oxidoreductases; Rats; Thymidine; Tritium

Topics: Acid Phosphatase; Age Factors; Alkaline Phosphatase; Animals; Brain Injuries; Esterases; Fluorescence; Histocytochemistry; Microscopy, Fluorescence; Rats; Staining and Labeling