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)

1. Receptor autoradiographic and histological techniques were used to investigate long-term changes in the gerbil brain following transient cerebral ischaemia. 2. Transient ischaemia was induced for 3 min and 10 min, and the animals were allowed to survive for 8 months. 3. Histological examination revealed that 3 min ischaemia caused neuronal damage and mild shrinkage only in the hippocampal CA1 sector. Ten minutes of ischaemia produced severe neuronal damage in the striatum and the hippocampal CA1 and CA3 sectors. Considerable shrinkage was seen in the hippocampus; the dentate gyrus, however, was not damaged. 4. Three minutes of ischaemia produced changes in the binding of [3H]-quinuclidinylbenzilate ([3H]-QNB), [3H]-muscimol, and [3H]-MK-801 in various brain regions, as determined autoradiographically. In contrast, [3H]-cyclohexladenosine ([3H]-CHA) and [3H]-PN200-110 ([3H]-isradipine) binding in the brain was unaltered. 5. Ten minutes of ischaemia resulted in a major loss of neurotransmitter receptors, especially in the hippocampus. The substantia nigra showed a significant reduction in [3H]-CHA binding, whereas the striatum, which was morphologically damaged, showed no significant changes in any of the neurotransmitter receptors examined. 6. The results demonstrated that long-term survival after transient cerebral ischaemia produced alterations in neurotransmitter receptors, especially in the hippocampal formation, where considerable shrinkage was noted. These results also suggest that the hippocampal damage was not static, but progressive.
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PMID:Long-term changes in gerbil brain neurotransmitter receptors following transient cerebral ischaemia. 133 Jan 76

We performed receptor autoradiography to determine sequential alterations in the binding of muscarinic cholinergic and adenosine A1 receptors and of a voltage dependent L-type calcium channel blocker 1 h-1 month after transient cerebral ischemia in the gerbil brain. [3H]Quinuclidinyl benzilate (QNB), [3H]cyclohexyladenosine (CHA) and [3H]PN200-110 were used to label muscarinic and adenosine A1 receptors and L-type calcium channels, respectively. Transient ischemia was induced for 10 min. [3H]QNB and [3H]CHA binding showed no significant alteration in selectively vulnerable areas at an early stage (1-24 h) of recirculation. However, the dentate molecular layer which was resistant to ischemia revealed a significant decrease in the [3H]CHA binding sites 24 h after ischemia. Thereafter, the [3H]QNB and [3H]CHA binding showed significant reduction in most of selectively vulnerable areas. Marked reduction was especially found in the dorsolateral part of striatum and the hippocampal CA1 sector which was the most vulnerable to ischemia. In contrast, [3H]PN200-110 binding showed a transient elevation in the hippocampal CA1 sector, the dentate molecular layer and the thalamus 1 h of recirculation. However, the striatum and neocortex revealed no alteration in the [3H]PN200-110 binding. Thereafter, the reduction in the [3H]PN200-110 binding was seen only in the dorsolateral part of the striatum and the hippocampal CA1 sector. The results suggest that transient cerebral ischemia can cause the alterations in the binding of muscarinic cholinergic and adenosine A1 receptors and of L-type calcium channel blocker in most of selectively vulnerable areas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postischemic alteration of muscarinic acetylcholine, adenosine A1 and calcium antagonist binding sites in selectively vulnerable areas: an autoradiographic study of gerbil brain. 166 8

This study examined brain-stem auditory evoked potentials response (BAEP) changes in the gerbil after temporary occlusion of the left carotid artery. Fourteen adult gerbils were subjected to unilateral left carotid ligation for 30 min. BAEPs were registered before and 5 min after occlusion, then 5 min, 60 min, 120 min, 24 h, 7 days and 28 days after release of the clip. Waves I (cochlear nerve), III (superior olivary complex) and V (inferior colliculus) were examined. Results were analysed using paired Student's t-test. Transient ischaemia increased latencies of waves I, III and V and the changes were more severe 5 min after release of the clip. In the gerbil, BAEPs might be a suitable method to study cerebral ischaemia.
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PMID:The auditory evoked potentials of gerbils after temporary occlusion of the left carotid artery. 204 13

The purpose of this study was to examine the distribution of neuronal damage following transient cerebral ischemia in the rat model of four-vessel occlusion utilizing light microscopy as well as 45Ca-autoradiography. Transient ischemia was induced for 30 min. The animals were allowed to survive for 7 d after ischemia. In the animals subjected to ischemia, the most frequently and seriously damaged areas were the paramedian region of hippocampus, the hippocampal CA1 sector, and the dorsolateral part of striatum, followed by the inferior colliculus, the substantia nigra, the frontal cortex, and the thalamus, which were moderate damaged. Furthermore, the cerebellar Purkinje neurons, the hippocampal CA4 sector, the medial geniculate body, and the hippocampal CA3 sector were slightly affected. 45Ca-autoradiographyic study also revealed calcium accumulation in the identical sites of ischemic neuronal damage, except for the frontal cortex. Regional cerebral blood flow during 10 min of ischemia was severely decreased in selectively vulnerable areas. The blood flow in the medial geniculate body, the substantia nigra, the inferior colliculus, and the cerebellum was less pronounced than that in the selectively vulnerable areas. The present study demonstrates that transient cerebral ischemia can produce significant neuronal damage not only in the selectively vulnerable regions, but also in the brainstem.
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PMID:Neuronal damage and calcium accumulation following transient cerebral ischemia in the rat. 209 66

The effects of 3-methyl-1-(5'-oxohexyl)-7-propylxanthine (propentofylline, HWA 285) on transient cerebral ischemia were studied in Mongolian gerbils by measuring the in vivo 31P nuclear magnetic resonance (NMR) spectra and cerebral water content. Transient ischemia was produced by bilateral common carotid artery occlusion for 30 min, which was followed by 60 min of reperfusion. Propentofylline (1, 2.5 or 30 mg/kg) or normal saline was administered intravenously at 2 min after the reperfusion. The 31P spectra during the occlusion showed a marked reduction in adenosine triphosphate (ATP) and phosphocreatine (PCr) with elevation of inorganic phosphate (Pi) in all groups. The intracellular pH (pHi) calculated from the chemical shift of Pi was markedly reduced in all groups. After the reperfusion, ATP, PCr, Pi and pHi gradually recovered towards the normal levels in the control group. In the 2.5 mg/kg propentofylline group, the energy recovery was significantly faster than in the controls. The cerebral water content measured at the end of reperfusion was significantly lower in the 2.5 mg/kg propentofylline group than in the controls. However, such cerebral protective effects were not observed in the 1 mg/kg and 30 mg/kg groups. The present results suggest that propentofylline may accelerate the energy recovery of the transiently ischemic brain and suppress the development of post-ischemic cerebral edema. The effects, however, were not dose-dependent in manner. The detailed mechanism of the effects requires further investigation.
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PMID:Effects of propentofylline on energy metabolism of the ischemic brain studied by in vivo 31P nuclear magnetic resonance spectroscopy. 251 Jul 44

The authors studied the ultrastructure of the brain tissue in "symptom negative" clawed jirds (M. unguiculatus) in the presence of permanent and transient circulatory ischemia caused by ligation of the right common carotid artery and by a 3-minute occlusion of the left common carotid artery which was unattended by any clinical manifestations signifying cerebral ischemia. The formation of oedema and dystrophic changes in the right hemisphere differed from that in the left one. Permanent ischemia was associated with the typical picture of hypoxic damage to the neural tissue with the development of cytotoxic oedema. Transient ischemia was predominantly characterized by an impairment of the blood-brain barrier with the development of marked vasogenic oedema. The study made it possible to closely follow the differences in the formation of an early stage of brain damage in permanent and transient ischemia and to establish the possibility of the damaging effect of blood recirculation in the hemisphere previously affected with ischemia.
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PMID:[Features of the ultrastructure of the brain tissue of Meriones unguiculatus after cerebral ischemia and postischemic recirculation]. 382 89

3 cases of transient global amnesia (TGA) are reported. Transient ischaemia is probably the cause of the condition in the majority of cases although other mechanisms, particularly epilepsy, may be responsible in some. TGA may not be reported by the patient and may be misdiagnosed as a psychiatric disturbance. An acute confusional or delirious state can also produce an episode of amnesia with inability to remember events which occurred during the period of cerebral dysfunction. In TGA, however, there is an acute and temporary failure to record events without the evidence of more generalised dysfunction which occurs in delirium. During the 3 episodes reported here the patients were able to carry on with their everyday activities and to complete structured tasks, such as the preparation of a meal. TGA appears, at least in some individuals, to carry the prognosis of transient cerebral ischaemia.
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PMID:Transient global amnesia. 730 49

To study the involvement of endogenous endothelin (ET) in the development of cerebral ischemia, we measured by radioimmunoassay brain tissue content of immunoreactive (ir)-ET-1 in a model of focal cerebral ischemia in the rat. Permanent occlusion of the middle cerebral artery (OMCA) was accompanied after 24 h by a progressive but marked elevation of ir-ET-1 in the ipsilateral compared with the contralateral hemisphere (119% after 24 h; 184% after 48 h and 459% after 72 h). The pial vessels and the arteries of the circle of Willis did not respond with ir-ET-1 production. The increase in ir-ET-1 content in tissues was first observed in the caudate nucleus (after 24 h) and later in the cortex (after 48 h), which was more variably injured. Transient ischemia followed by recirculation led to a slight increase of ir-ET-1, which also appeared after 24 h of recirculation. This study demonstrates that during permanent OMCA, the tissue content of ir-ET-1 markedly and progressively increases, whereas less severe ischemia (transient) is accompanied by a modest elevation of ir-ET-1 levels. These results suggest that endogenous ir-ET-1 production is involved in the development and the severity of ischemic injury.
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PMID:Elevated tissue endothelin content during focal cerebral ischemia in the rat. 750 72

To determine whether presynaptic sites are resistant to cerebral ischaemia, we investigated the postischaemic alteration in [3H]hemicholinium-3 binding as a sensitive marker of presynaptic cholinergic terminals in the gerbil brain between 1 h and 7 days after recirculation using receptor autoradiography. Transient ischaemia was induced for 10 min. [3H]hemicholinium-3 binding was unchanged in the frontal cortex, striatum and hippocampus throughout the recirculation periods. Our histological study revealed conspicuous neuronal damage in the frontal cortex, striatum, hippocampal CA1 sector and hippocampal CA3 sector after ischaemia. The present study demonstrates that presynaptic sites in selectively vulnerable areas can maintain their structural components although postsynaptic neurones are clearly degenerated. Thus our findings support the hypothesis that presynaptic sites are particularly resistant to ischaemia, but postsynaptic sites are vulnerable.
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PMID:Alteration of [3H]hemicholinium-3 binding in the post-ischaemic gerbil brain. 776 64

The effect of dynorphin A-(1-13), an endogenous kappa-opioid receptor agonist, on memory dysfunctions induced by transient cerebral ischemia in mice was investigated by using three different tasks, namely, spontaneous alternation, elevated plus-maze performance, and passive avoidance behavior. Transient ischemia produced a marked memory dysfunction in mice, as assessed in the three tasks, which were carried out consecutively 1 to 3 days after the ischemic insult. The i.c.v. injection of dynorphin A-(1-13) before the ischemic insult potently prevented the impairment of spontaneous alternations, the prolongation of transfer latency in the elevated plus-maze and the shortening of step-through latency in the passive avoidance task induced by transient ischemia. Dynorphin A-(1-13) (10 micrograms), however, did not affect the body temperature of the sham-operated or the ischemic mice. The protective effect of dynorphin A-(1-13) (10 micrograms) on ischemia-induced memory dysfunctions observed in the three tasks was almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms, i.c.v.), a kappa-selective opioid receptor antagonist. These results suggest that dynorphin A-(1-13) prevents memory dysfunctions in ischemic mice through the activation of kappa-opioid receptors.
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PMID:Dynorphin A-(1-13) potently prevents memory dysfunctions induced by transient cerebral ischemia in mice. 809 64


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