Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of acute perinatal ischemia-hypoxia on fetal liver and brain energy metabolism, fetal brain total free fatty acid concentration and subsequent offspring behavior were investigated in rats. Ischemia-hypoxia was induced at term either by ligation of the uterine blood vessels or submersion of the entire uterine horn in warmed saline. Fetuses of the adjacent horn served as within-dam controls for all assessments and fetuses of dams which had not undergone the surgical stress served as independent controls for enzyme assays. Ischemia-hypoxia was associated with reduced activity of fatty acid synthase in the liver and brain. Total free fatty acid concentration significantly increased in the fetal hypoxic brain. Pups not used for enzyme analyses were cross-fostered for behavioral assessments. Relative to the enzymatic alterations, there were few behavioral alterations associated with ischemia-hypoxia. At postnatal day 30, rats made hypoxic by ligation of the uterine blood vessels had decreased caudate nucleus and brain stem weights relative to within-dam controls. At postnatal day 85, rats made hypoxic by submersion of the uterine horn had decreased olfactory bulb weight. The results of this study indicate an initial acute response to a brief period of ischemia-hypoxia at term pregnancy in the fetal rat brain and liver.
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PMID:Effects of ischemia-hypoxia induced by interruption of uterine blood flow on fetal rat liver and brain enzyme activities and offspring behavior. 888 73

Cortical venous drainage has been described as one of the major risk factors for dural arteriovenous fistula, which may induce venous hypertension leading to venous ischemia or intracerebral hemorrhage. However, it is rather rare to observe cortical venous drainage manifesting in this way in the cavernous sinus region. We report a case of a 55-year-old gentleman with a right cavernous dural arteriovenous fistula, presenting with conjunctival chemosis, exophthalmus and ocular hypertension on the affected side. Magnetic resonance imaging showed a small intracerebral hemorrhage in the right frontal lobe. Cerebral angiography revealed a dural arteriovenous fistula in the right cavernous sinus draining into the right olfactory vein via the uncal vein, as well as into the superior and inferior ophthalmic veins. This unusual cortical venous reflux was thought to be consistent with the intracerebral hemorrhage found on the magnetic resonance imaging. The patient underwent transvenous embolization for the dural arteriovenous fistula using an inferior petrosal catheterization into the uncal vein was difficult, and the cortical venous reflux through the vein seemed to be slight. However, extravasation of the contrast material occurred in the right frontal lobe after obliteration of the ophthalmic veins during the procedure. The cause of the extravasation was suspected to be the same olfactory vein that had been involved in the previous intracerebral hemorrhage. The obliteration of the dural fistula was continued rapidly, and the fistula disappeared after the embolization. Neurologically, the patient had no noticeable troubles, except for a mild headache. The pretreatment symptoms were alleviated within several days, and the patient was discharged in a week. We emphasize the following points from this rare case in order to facilitate a safer procedure during transvenous embolization for cavernous dural arteriovenous fistula. It is important to obliterate the cortical venous drainage as early as possible, even if the reflux is small or the catheterization is difficult. Repeated, careful sinography is useful for the evaluation of the drainage pattern at certain stages during the transvenous embolization procedure.
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PMID:[A case of cavernous dural arteriovenous fistula resulting in intracerebral extravasation during transvenous embolization]. 926 67

The expression of immediate early genes (IEG) has been documented in the brain after various kinds of insults such as ischemia and hypoxia. To determine whether acute carbon monoxide intoxication (ACOI) might trigger IEG expression, adult ddY mice were subjected to carbon monoxide exposure at a rate of 30 mL/min for 35 seconds. The levels of NGFI-B, c-fos, and c-jun mRNA were determined by Northern blot analysis. A time-course study in the cerebral cortex indicated that the induction of NGFI-B, c-fos, and c-jun mRNA started as early as 15 minutes, reached a peak at 30 minutes, and returned to the basal level at 1 hour after the ACOI. In addition, the temporal feature of the induction of these IEG mRNA in the hippocampus was very similar to that in the cerebral cortex. Examination of brain regions at 30 minutes after the ACOI revealed a significant induction of NGFI-B mRNA in the cerebellum, thalamus-hypothalamus, brainstem. as well as in the cortex and hippocampus, but not in the striatum or olfactory bulb. Furthermore, the neuroanatomical distribution of c-fos mRNA at 30 minutes after the ACOI was very similar to that of the NGFI-B mRNA. The widespread distribution of these IEG in the brain, especially in the cerebellum and brainstem, indicates that the major cause for the triggering of IEG expression in the brain by the ACOI might be a diffuse hypoxia. These findings show for the first time the temporal and spatial expression of IEG in the brain after ACOI.
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PMID:NGFI-B, c-fos, and c-jun mRNA expression in mouse brain after acute carbon monoxide intoxication. 927 Apr 94

Brain slices (olfactory cortex, fronto-parietal cortex and hippocampus) taken from normal or microencephalic rats, obtained by gestational administration of the DNA-alkylating agent methylazoxymethanol acetate (MAM), were subjected to in vitro simulated ischemia or exposed to glutamate (5 mM) or kainate (1 mM). All these neurotoxic insults resulted in decreased viability of the slices, as quantitatively assessed by decrease in the rate of protein synthesis. Hippocampal slices subjected to ischemia and olfactory cortex slices exposed to glutamate or kainate were significantly less sensitive to the neurotoxic insult in microencephalic rats than in controls. The increased efflux of neurotransmitter amino acids (glutamate, aspartate and GABA) in the medium from slices subjected to ischemia or exposed to kainate, showed no significant differences among microencephalic and control rats. The present results suggest that the decreased excitotoxic sensitivity of microencephalic rats is, at least in part, related to intrinsic structural and/or functional alterations of some brain regions which undergo decrease in size as a consequence of the gestational treatment.
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PMID:Ischemic and excitotoxic damage to brain slices from normal and microencephalic rats. 932 38

The histaminergic neuron system is located in the posterior hypothalamus as a tuberomammillary nucleus (TM) and sends nerve fibers with varicosities to almost all regions of the brain from the olfactory bulb to the spinal cord, suggesting that this neuron system is involved in the control of the activities of the whole brain. We examined the effects of pharmacological manipulations of the histaminergic neuron system on various kinds of invasive stimuli, such as methamphetamine behavioral sensitization (reverse tolerance), neuronal cell death caused by brain ischemia and electroconvulsive shock. Nerve degeneration caused by chemical and physical denervation caused an increase in H3 receptors in the postsynaptic sites. It seems likely that histamine functions in a direction to protect against various stimuli to maintain homeostasis, which is in good agreement with the morphological characteristics described above.
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PMID:[Histaminergic neuron system and neural plasticity]. 936 65

Estrogen replacement therapy in postmenopausal women is associated with a decreased mortality and morbidity from stroke. The present study was undertaken to investigate the effects of estrogen on endothelial cell glucose transporter 1 (GLUT 1) and on the cell viability during focal ischemia in a rat model. Female rats were ovariectomized (OVX) and 2 weeks later 17beta-estradiol (E2) was injected subcutaneously at a dose of 100 microg/kg 2 h before unilateral middle cerebral artery (MCA) occlusion. Ischemic lesion size was quantified using 2,3,5-triphenyl tetrazolium chloride (TTC) staining and GLUT 1 protein was analyzed by Western blotting. E2 treatment decreased ischemic lesion size in slices taken at 9 and 11 mm posterior from the olfactory bulb by 46.3% and 44.1%, respectively (P < 0.05). GLUT 1 protein decreased in both OVX and E2 groups by 24.6% and 22.7% respectively (P < 0.05) compared with the non-lesioned side in the core ischemic region, including the basal ganglia. GLUT 1 protein was increased in the E2-treated group compared with the control group (23.3%, P < 0.05) in the penumbral ischemic region of the cortex. Primary rat brain capillary endothelial cell (BCEC) cultures were established as an in vitro model for ischemic effects on endothelial cells. Estrogen reduced BCEC loss by 35.9%, 28.4% and 23.5% (P < 0.05) when glucose in the culture medium was reduced to 50%, 20% and 10%, respectively; and by 28.4% and 18.4% (P < 0.05) following 1 or 4 h of anoxia, respectively. This study demonstrates that estrogen treatment increases GLUT 1 transporters and protects BCEC loss which may in turn reduce focal ischemic brain damage.
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PMID:Effects of 17beta-estradiol on glucose transporter 1 expression and endothelial cell survival following focal ischemia in the rats. 941 67

To study the distribution of ciliary neurotrophic factor (CNTF) in the rat brain under physiological as well as pathological conditions, a sensitive sandwich enzyme linked immunoassay (EIA) for rat CNTF was developed using rabbit anti-CNTF antibody. This method detected as little as 10 pg ml-1 CNTF with a good linearity and accuracy. Analysis of various regions of rat brain and peripheral nerves showed a high content of CNTF in the sciatic nerves, spinal cord, optic nerves, and olfactory bulb. Transient focal ischemia of rat brain caused by middle cerebral artery occlusion significantly and specifically increased CNTF levels in the cerebral cortex and hippocampus regions in the ischemic hemisphere.
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PMID:Increase of ciliary neurotrophic factor (CNTF) in the ischemic rat brain as determined by a sensitive enzyme-linked immunoassay. 942 58

Mice lacking the epidermal growth factor receptor (EGFR) exhibit strain-dependent phenotypes ranging from placental to postnatal skin, lung and brain defects. After birth, all mutant mice develop a progressive neurodegeneration in the frontal cortex, olfactory bulb and thalamus, characterized by massive apoptosis and upregulation of c-fos. These defects occur in a strain-independent manner, since neither rescue of the placental phenotype by aggregation of diploid 129/Sv EGFR mutant and tetraploid wild-type embryos, nor promotion of lung maturation by transplacental dexamethasone administration alters the course of neurodegeneration. VEGF is not induced during the degenerative process, excluding hypoxia and ischemia as causes of cell death. A migratory disorder is detected in the hippocampus with nests of ectopic neurons, which are also apoptotic. Cerebral cortices from EGFR mutants contain lower numbers of GFAP positive astrocytes, which display reduced proliferation in vitro. Since EGFR is expressed in the affected cell-types, these results define a specific function for EGFR in the proliferation and/or differentiation of astrocytes and in the survival of postmitotic neurons.
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PMID:A strain-independent postnatal neurodegeneration in mice lacking the EGF receptor. 945 Sep 97

Focal cerebral ischemia is associated with expression of both inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), enzymes whose reaction products contribute to the evolution of ischemic brain injury. We tested the hypothesis that, after cerebral ischemia, nitric oxide (NO) produced by iNOS enhances COX-2 activity, thereby increasing the toxic potential of this enzyme. Cerebral ischemia was produced by middle cerebral artery occlusion in rats or mice. Twenty-four hours after ischemia in rats, iNOS-immunoreactive neutrophils were observed in close proximity (<20 micrometer) to COX-2-positive cells at the periphery of the infarct. In the olfactory bulb, only COX-2 positive cells were observed. Cerebral ischemia increased the concentration of the COX-2 reaction product prostaglandin E2 (PGE2) in the ischemic area and in the ipsilateral olfactory bulb. The iNOS inhibitor aminoguanidine reduced PGE2 concentration in the infarct, where both iNOS and COX-2 were expressed, but not in the olfactory bulb, where only COX-2 was expressed. Postischemic PGE2 accumulation was reduced significantly in iNOS null mice compared with wild-type controls (C57BL/6 or SV129). The data provide evidence that NO produced by iNOS influences COX-2 activity after focal cerebral ischemia. Pro-inflammatory prostanoids and reactive oxygen species produced by COX-2 may be a previously unrecognized factor by which NO contributes to ischemic brain injury. The pathogenic effect of the interaction between NO, or a derived specie, and COX-2 is likely to play a role also in other brain diseases associated with inflammation.
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PMID:Interaction between inducible nitric oxide synthase and cyclooxygenase-2 after cerebral ischemia. 972 13

Protein biosynthesis is mainly under the control at the level of gene transcription in eukaryotes. Transcription factors are nuclear proteins with abilities to modulate the activity of RNA polymerase II which is responsible for the formation of messenger RNA from double stranded DNA in the cell nuclei. Binding of a radiolabeled oligonucleotide probe for the transcription factor activator protein-1 (AP1) was transiently potentiated 1 to 6 h after the recirculation of blood supply in the thalamus and striatum, but not in the entorhinal cortex, olfactory bulb, frontal cortex, cerebellar cortex and medulla-pons, in gerbils with transient global forebrain ischemia for 5 min, in addition to the hippocampal subregions. The ischemic insult not only increased the immunoreactivity with an antibody against cyclic AMP response element binding protein (CREB) phosphorylated at serine133, but also induced the expression of both c-Jun and c-Fos family proteins 3 h after the recirculation in the thalamus. Limited proteolysis by Staphylococcus aureus (S. aureus) V8 protease revealed the expression of different partner proteins of AP1 in response to ischemic signals in the thalamus. Moreover, ischemia for 2 min led to more prolonged elevation of AP1 binding in the thalamus at least up to 12 h after the reperfusion than that seen with ischemia for 5 min. These results suggest that potentiation of AP1 DNA binding may at least in part involve mechanisms associated with the expression of c-Fos protein through phosphorylation of CREB at serine133 in the thalamus of gerbils with ischemia.
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PMID:Correlation between potentiation of AP1 DNA binding and expression of c-Fos in association with phosphorylation of CREB at serine133 in thalamus of gerbils with ischemia. 973 29


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