acid-phosphatase and Cerebral-Infarction

acid-phosphatase has been researched along with Cerebral-Infarction* in 2 studies

Other Studies

2 other study(ies) available for acid-phosphatase and Cerebral-Infarction

ArticleYear
Histochemical and morphometric investigation of the pathogenesis of acute brain infarction in primates.
    Acta histochemica. Supplementband, 1992, Volume: 42

    The right medial cerebral artery of 25 primates (Macaca radiata) was occluded transorbitally with an atraumatic clip. The time courses of infarct volume and capillary morphometric changes in the ischemic lenticular nucleus, caudate nucleus and insular cortex were then determined. Volume changes of ischemic foci were studied morphometrically using an enzyme histotopochemical acid phosphatase stain. During the first 4 hours extension (or spread) of the ischemic area was small and constant. Over the next hours, the ischemic focus increased in volume, becoming maximal in the lenticular nucleus in 24 hours and in the caudate nucleus in 48 hours. In the lenticular nucleus, edema developed 4 hours after onset of ischemia and was characterized by a decrease in capillary diameter and an increase in mean intercapillary distance. In the caudate nucleus and insular cortex, in the first hours after clipping the medial cerebral artery, capillary diameter and volume increased and intercapillary distance decreased. The data demonstrate that the therapeutic window of brain infarct treatment is during the first 4-6 hours after occlusion of the medial cerebral artery.

    Topics: Acid Phosphatase; Acute Disease; Alkaline Phosphatase; Animals; Brain; Capillaries; Cerebral Arteries; Cerebral Infarction; Histocytochemistry; L-Lactate Dehydrogenase; Macaca radiata

1992
Olivary hypertrophy: histochemical demonstration of hydrolytic enzymes.
    Neurology, 1980, Volume: 30, Issue:5

    Of four patients with palatal myoclonus, three had infarcts resulting from atherosclerosis, and one had cerebral emboli from a left atrial myxoma. Three specimens showed lesions in the brainstem and bilateral hypertrophy of the inferior olivary nuclei; the fourth revealed unilateral olivary changes caused by an infarct in the contralateral dentate nucleus. After incubation for acetylcholinesterase, neuropilar and capillary wall staining were absent or much reduced, but there was increased denisty of reaction product in the neuronal cell bodies and in numerous tortuous dendrites. Methods for acid phosphatase showed strong activity in the dendrites and glomeruloid structures of the diseased olives. Reactions for nonspecific esterase indicated dendritic expansion and reduced staining density in nerve cell bodies, but augmented glial reactivity.

    Topics: Acetylcholinesterase; Acid Phosphatase; Adenosine Triphosphatases; Adult; Aged; Butyrylcholinesterase; Cerebral Hemorrhage; Cerebral Infarction; Esterases; Female; Humans; Hypertrophy; Male; Middle Aged; Myoclonus; Olivary Nucleus; Phosphoric Monoester Hydrolases

1980