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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathophysiological feature of brain ischemia-infarct was investigated using immunohistochemistry and Gallyas' silver staining after transient ischemia of the middle cerebral artery (MCA) in the rat. A very strong IgG infiltration with clear-cut borders was detected at one to 3 days in ischemic core areas (lateral striatum and adjacent cortex) that fell into porencephaly later. Complement factor C3 (C3) immunoreactivity (IR) appeared similarly while albumin IR more diffusely. Microglial activation could be observed at 1 day while rounded leukocyte-like elements at 3 days after reperfusion. Data suggest that the early appearance of the IgG/C3 IR bears particular importance after transient MCA ischemia as it could predict the ensuing porencephaly in the chronic stage.
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PMID:Appearance of immunoglobulin G and complement factor C3 in the striatum after transient focal ischemia in the rat. 819 Mar 58

Transient ischemia-induced perturbations in calcium homeostasis have been proposed to lead to pathological activation of the cysteine protease calpain I and subsequent delayed neuronal death in the CA1 region of hippocampus. We report here on the design and characterization of antibodies selective for calpain-generated fragments of brain spectrin, and their use for immunoblot and immunohistochemical analyses of calpain activation following cerebral ischemia in the gerbil. Although spectrin was susceptible to degradation in vitro by many mammalian proteases, only calpain degraded spectrin to generate fragments immunoreactive with the antibodies. Following 5 min of global ischemia, immunoreactivity for calpain-degraded spectrin was rapidly (within 30 min) and markedly elevated in the perikarya and dendrites of several populations of forebrain neurons. The rapid calpain activation was completely prevented by the NMDA receptor antagonist MK-801. At later times postischemia, but prior to frank neuronal necrosis, calpain-degraded spectrin was restricted to hippocampal area CA1 pyramidal neurons. Silver impregnation histochemistry confirmed that neuronal damage was confined to area CA1. The results indicate that while nonpathological NMDA receptor stimulation can activate calpain, only those neurons showing sustained calpain activation are destined to die.
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PMID:Immunolocalization of calpain I-mediated spectrin degradation to vulnerable neurons in the ischemic gerbil brain. 820 97

Six thalassaemic patients had a distinct clinical syndrome characterized by progressive ischemia of the lower extremities, with ascending arteritis and thrombosis of the main arteries of the lower limbs. With periodic acid Schiff and Gomori's methenamine silver staining a large number of hyphae were revealed in the arterial wall and the outer part of the thrombus. Pythium insidiosum was isolated from 3 patients. The clinical course of the disease was progressive gangrene of the extremities and the patients invariably died when the infectious process reached the bifurcation of the aorta. There is no effective antimicrobial agent for the syndrome and radical amputation was the only method to ensure survival of the patients. P. insidiosum infection should be considered in thalassaemic patients with leg ulcers or arterial occlusion of the lower limbs.
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PMID:Fatal arteritis due to Pythium insidiosum infection in patients with thalassaemia. 823 97

Much of the work on forebrain ischemia in the hippocampus has focused on the phenomenon of delayed neuronal death in CA1. It is established that dentate granule cells and CA3 pyramidal cells are resistant to ischemia. However, much less is known about interneuronal involvement in CA3 or ischemic injury in the dentate hilus other than the fact that somatostatin neurons in the latter lose their immunoreactivity. We combined two sensitive methods--heat-shock protein (HSP72) immunocytochemistry and a newly developed Gallyas silver stain for demonstrating impaired cytoskeletal elements--to investigate the extent of ischemic damage to CA3 and the dentate hilus using the four-vessel-occlusion model for inducing forebrain ischemia. HSP72-like immunoreactivity was induced in neuronal populations previously shown to be vulnerable to ischemia. In addition, a distinct subset of interneurons in CA3 was also extremely sensitive to ischemia, even more so than the CA1 pyramidal cells. These neurons are located in the stratum lucidum of CA3 and possess a very high density of dendritic spines. In silver preparations, they were among the first to be impregnated as "dark" neurons, before CA1 pyramidal cells; microglial reaction was also initiated first in the stratum lucidum of CA3. Whereas CA1 damage was most prominent in the septal half of the hippocampus, hilar and CA3 interneuronal damage had a more extensive dorsoventral distribution. Our results also show a far greater extent of damage in hilar neurons than previously reported. At least four hilar cell types were consistently compromised: mossy cells, spiny fusiform cells, sparsely spiny fusiform cells, and long-spined multipolar cells. A common denominator of the injured neurons in CA3 and the hilus was the presence of spines on their dendrites, which in large part accounted for the far greater number of mossy fiber terminals they receive than their non-spiny neighbors. We suggest that the differential vulnerability of neuronal subtypes in these two regions may be attributed to their extremely dense innervation by the mossy fibers and/or the presence of non-NMDA receptor subtypes that are highly permeable to calcium. In addition, early impairment of these spiny CA3 cells and hilar neurons after ischemia may be causal to delayed neuronal death in the CA1 pyramidal cells.
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PMID:Vulnerability of mossy fiber targets in the rat hippocampus to forebrain ischemia. 836 55

The damaging effects from transient forebrain ischemia may be a result of excessive excitability or loss of inhibitory influences. In the brain, GABA acts as the major inhibitory neurotransmitter and its loss may be an important factor leading to delayed neuronal damage in the substantia nigra reticulata (SNr). In this study, we looked at the protective effects of muscimol, a GABA A agonist in a gerbil model of repetitive forebrain ischemia. For cerebral ischemia, we used three episodes of 2 min with a reperfusion period of 1 h between the insults. Histological evaluations were done 7 days after the insult using silver degeneration staining. Muscimol was infused into the third ventricle continuously for 7 days beginning just prior to the insult. There were a total of 20 animals, 12 treated with muscimol and the other 8 serving as controls. At 7 days, there was significant protection in the cortex (P = 0.007), hippocampus [CA1 (P = 0.01), CA4 (P = 0.015)], substantia nigra reticulata (P = 0.007), striatum (P = 0.049), and thalamus (P = 0.012). All statistical comparisons were done using nonparametric tests (Mann-Whitney U test). Our study shows that potentiation of inhibitory mechanisms may be important mechanisms of neuronal protection from the effects of repetitive ischemia and the effects are not limited to the SNr. Further studies are needed to better understand their mechanism of action.
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PMID:GABA agonist "muscimol" is neuroprotective in repetitive transient forebrain ischemia in gerbils. 840 90

Post-ischemic treatment of di-Calciphor (16,16'-dimethyl-15- dehydroprostaglandin B1) significantly improves animal survival and prevents ischemia-induced neurodegeneration of vulnerable forebrain regions assessed with histochemical and biochemical techniques in gerbils. Neuronal degeneration seen by Cresyl violet staining and silver impregnation in the CA1 sector of the hippocampus and the dorso-lateral sector of the striatum was significantly reduced in animals treated with di-Calciphor. In addition, the early onset of selective degradation of calpain I substrates spectrin and microtubule-associated protein (MAP2) in these same vulnerable regions was prevented. The lack of adverse side effects may facilitate the potential therapeutic use of this drug in preventing neuronal damage caused by stroke.
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PMID:Neuroprotective activity of dimer of 16,16'-dimethyl-15-dehydroprostaglandin B1 (di-Calciphor) in cerebral ischemia. 846 94

Brief periods of forebrain ischemia result in consistent damage in the hippocampus in gerbils. This damage can be attenuated by free radical scavengers, glutamate antagonists and GABA agonists. Most of the work with cerebral protection has been done with agents infused prior to the insult. In this experiment we tested clomethiazole, a GABA agonist, as a neuroprotective agent 1 and 4 h after a 5 min ischemic insult (bilateral carotid occlusion) in gerbils. Damage was assessed using silver staining techniques at 7 days after the insult. There were 10 animals in each group. Clomethiazole was given subcutaneously at a dose of 100 mg/kg. Compared to controls, there was significant protection in the CA1 (P < 0.01) and CA4 (P < 0.01) regions of the hippocampus at 1 and 4 h after the ischemic insult. GABAergic agents may play an important role in neuronal protection when used after ischemic insults.
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PMID:Clomethiazole protects the brain in transient forebrain ischemia when used up to 4 h after the insult. 855 72

The histoblot immunostaining technique for locating and characterizing amyloidogenic proteins was used to obtain information about the relationship of cerebral ischemia/hypoxia to the accumulation of amyloid beta protein (A beta). We investigated brains of 131 subjects (ages 25-94 years, mean 72 years). Three distribution patterns of A beta immunoreactivity were identified: (1) colocalization with diffuse and neuritic plaques of Alzheimer's disease (AD) and aging; (2) diffuse punctuate deposits in the cerebral cortex in association with small vessel cerebral vascular disease ; and (3) cerebral cortical accumulation localized to arterial boundary zones and other regions susceptible to ischemic/hypoxic injury designated "stress-induced deposits" (SID). SID were not identified in tissue sections by immunohistochemical, Congo red or Bielschowsky silver techniques; no histological abnormalities were present in adjacent formalin-fixed tissue sections, SID occurred in subjects with histories of cerebral ischemia, and severe orthostatic hypotension. There was also an association with aging in general and with the incidence of neuritic plaques specifically. These latter findings are consistent with the hypothesis that brain ischemia/hypoxia plays a role in the pathogenesis of AD.
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PMID:Ischemic stress induces deposition of amyloid beta immunoreactivity in human brain. 856 Sep 78

Using a silver impregnation (argyrophil III) and immunohistochemistry, acute cytopathic features after cerebral ischemia were investigated. Additionally, functional recovery and interconnection between the host and graft was also explored after neural graft. Animals were embolized in unilateral middle cerebral artery for 1 h. Argyrophil III method demonstrated "collapsed" dark neurons in the striatum, cortex, reticular thalamus, amygdala, and hypothalamus on ischemic side. These neurons exhibited characteristic shrunken somata with corkscrew-like dendrites, suggesting changes in cytoskeletal protein. In the above mentioned areas, the loss of immunoreactivity for mu-calpain proenzyme and microtubule-associated protein 2 was also detected. Neural graft into the ischemic striatum was made 2 weeks after the ischemia paradign. The grafted striatal cells were prepared from E15 fetuses to make cell suspension marked by rhodamine-labeled latex microspheres. Methamphetamine-evoked rotations were detected after ischemia. These motor alterations were reduced gradually but significantly at 8 weeks after the graft. Interconnecton between the host and grafted cells was then studied in a brain slice preparation after loading fura-2 AM. About 10% of grafted cells tested from rats that showed motor amelioration exhibited [Ca2+]i increase to the electrical stimulation applied to the neighboring host tissue. Data indicate that, in the very early stage after ischemia, cytoskeletal damages, especially on microtubules, started and this would lead to later infarct. The graft survived in the ischemic striatum having connections with the host, and this might be partly involved in the amelioration of motor function.
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PMID:Early cytopathic features in rat ischemia model and reconstruction by neural graft. 863 48

Argyrophil III silver impregnation is a very sensitive method to detec t the early damage to neurons following brain ischemia. The argyrophil III staining and microtubule-associated protein 2 (MAP2) immunocytochemistry were performed on PC12D cells and MAP2C cDNA-transfected COS7 cells to detect the changes cytoskeletal proteins (microtubules/MAP2). After exposing these cells to simulated ischemic condition (oxygen and/or glucose free), the correlation between the appearance of the argyrophilia and the disappearance of MAP2 was investigated. The PC12D cells expressed very low MAP2 and became argyrophilic very easily depending on the degree of the ischmeia-like insult, whereas MAP2C cDNA-transfected COS7 cells expressed a higher level of MAP2C and were resistant to argyrophilia, although the diameter of their immunoreactive processes became thinner. Thus, when MAP2C is expressed at a higher level, cells became resistant to argyrophilia, suggesting a correlation between the argyrophilia and the damage on microtubules and MAPs.
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PMID:Microtubule-associated protein 2 expressing COS7 cells are resistant to argyrophilia under oxygen- and glucose-free condition. 863 51


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