Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mongolian gerbils subjected to 5-min cerebral ischemia by common carotid artery ligation were decapitated after 24, 48, 72 and 96 h of survival to investigate the immunoreactivity of astroglia in the hippocampus. The sections from formalin-fixed, paraffin-embedded brains were stained histologically and with ABC method (Hsu et al. 1981). Control animals (normal and shame-operated) presented positive GFAP immunostaining in corpus callosum, in subventricular regions, in temporal subcortical white matter, in fimbria hipocampi and perivascularly in stratum lacunosum-moleculare. Experimental animals, independently of postischemic survival time showed various individual GFAP reactivity. Differences concerning the number and localization of immunoreactive astrocytes in both cerebral hemispheres of the same animal stressed the asymmetry of the reaction. The authors did not observe any accumulation of reactive astrocytes in the area of synaptic terminals of glutaminergic fibers (mossy fibers, Schaffer's collaterals) or in the neighbourhood of CA1 and CA3 sectors. In particular, there was complete lack or only sporadic reactive astrocytes among pyramidal neurons of CA1 and among granular cells of dentate gyrus in all examined animals.
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PMID:Immunoreactivity of astroglia in the hippocampus of the Mongolian gerbil during short survival following brief ischemia. 134 Sep 15

The effects of cerebral ischaemia by carotid artery occlusion and of a ganglionic blocking agent (Arfonad) on cardiac output and regional blood flows were studied after 15 min of haemorrhagic hypotension (mean arterial pressure 50 mmHg) in the rat. The microsphere technique was used for blood flow determinations. Animals subjected to haemorrhagic hypotension and simultaneous carotid artery occlusion (group BC) exhibited a stronger immediate vasoconstrictor response than animals subjected to haemorrhagic hypotension only (group B) and more blood had to be withdrawn to achieve stable hypotension at 50 mmHg (2.6 +/- 0.1 vs. 2.2 +/- 0.4 ml per 100 g body weight (body wt); P less than 0.05). However, group B showed the same decrease in cardiac output as group BC, but the blood flows of the kidneys, spleen, intestine, liver and skin were less deranged at the end of the hypotensive period. Groups B and BC exhibited similar intestinal ischaemic mucosal damage, measured as leakage of [125I]albumin. When induction of haemorrhagic hypotension was combined with ganglionic blockade administration (Arfonad) and carotid artery occlusion (group ABC), significantly less blood had to be withdrawn than in groups BC (1.6 +/- 0.2 vs. 2.6 +/- 0.1 ml per 100 g body wt; P less than 0.05). The blood flows of the kidneys, small intestine, liver, spleen and skin were less compromised in group ABC. In addition, group BC had more profound metabolic acidosis and were more haemoconcentrated than group ABC; moreover, group BC, tended to be hypoglycaemic and showed intestinal mucosal damage, whereas neither of these effects occurred in group ABC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of carotid artery occlusion and ganglionic blockade on regional blood flows and intestinal damage after haemorrhagic hypotension in the rat. 287 9

The study was performed on 98 Mongolian gerbils. Cerebral ischemia was evoked by ligation of both common carotid arteries for 5 min. After five postischemic days the animals were decapitated, brains fixed, paraffin section stained with histological methods and for GFAP with ABC method. The investigated animals (ca 18%) presented asymmetrical morphological lesions of the CA1 hippocampal sector showing irregular loss of neurons in both cerebral hemispheres. GFAP immunostaining demonstrated various astroglial proliferation in asymmetrical lesions of CA1 sector. In partial injury to CA1 neurons the astrocytes in stratum (s) pyramidale were single but their number still increased when total loss of pyramidal neurons occurred. Except s. lacunosum moleculare the number of GFAP-positive astrocytes in the remaining layers of dorsal hippocampus presented a direct relationship with the intensity of morphological changes and was highest when 70% loss of pyramidal cells was observed.
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PMID:Immunoreactivity of astroglia after brief ischemia resulting in asymmetrical damage to the hippocampal CA1 sector in the Mongolian gerbil. 792 14

Physical and chemical constraints imposed by the periinfarct glial scar may contribute to the limited clinical improvement often observed after ischemic brain injury. To investigate the role of some of these mediators in outcome from cerebral ischemia, we treated rats with the growth-inhibitory chondroitin sulfate proteoglycan neurocan, the growth-stimulating heparan sulfate proteoglycan glypican, or the chondroitin sulfate proteoglycan-degrading enzyme chondroitinase ABC. Neurocan, glypican, or chondroitinase ABC was infused directly into the infarct cavity for 7 d, beginning 7 d after middle cerebral artery occlusion. Glypican and chondroitinase ABC reduced glial fibrillary acidic protein immunoreactivity and increased microtubule-associated protein-2 immunoreactivity in the periinfarct region, and glypican- and chondroitinase ABC-treated rats showed behavioral improvement compared with neurocan- or saline-treated rats. Glypican and chondroitinase ABC also increased neurite extension in cortical neuron cultures. Glypican increased fibroblast growth factor-2 expression and chondroitinase ABC increased brain-derived neurotrophic factor expression in these cultures, whereas no such effects were seen following neurocan treatment. Thus, treatment with glypican or enzymatic disruption of neurocan with chondroitinase ABC improves gross anatomical, histological, and functional outcome in the chronic phase of experimental stroke in rats. Changes in growth factor expression and neuritogenesis may help to mediate these effects.
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PMID:Intracerebral chondroitinase ABC and heparan sulfate proteoglycan glypican improve outcome from chronic stroke in rats. 2261 73