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)

After the middle cerebral artery of rats was occluded, changes in the content of 14 free amino acids and the activity of antioxidant enzymes in the ischemic striatum were assessed with respect to the duration of ischemia. Glu and Asp levels were significantly reduced by 60 min of ischemia, GABA was increased by 30 and 60 min and Ala was increased by 5, 15, and 30 min. During ischemia, the levels of striatal Gln, Asn, Ser, Tau, Gly and Pro were found to be normal. In comparison with the sham-operated rats, the changes in the content of Thr, His, Arg and Tyr were inconclusive, since the effect of operative stress could not be ruled out on such occasion. Concomitantly, the Zn-Cu superoxide dismutase and glutathione peroxidase activity were significantly reduced by 30 min of ischemia. It revealed that the reduced capacity to scavenge the oxygen free radicals occurred during the early stage of cerebral ischemia. The above changes of Glu, Gln, GABA and Pro level might be considered as the final outcome of the decrease of glutamate synthesis, the acceleration of its conversion to GABA, and the extracellular leakage of glutamate. According to our data, the oxygen free radicals might be involved in the evolution of primary neuronal damage at the ischemic striatum.
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PMID:[Mechanism of neuronal damage caused by cerebral ischemia]. 133 25

A 74-year-old right-handed man with multiple cerebral infarction who presented with dementia simulating dementia of Alzheimer type (DAT) is reported. He had been well until April 20, 1987 when he developed transient right hand palsy lasting overnight. Eleven days later, he became confused, disorientated, and amnestic. He was admitted to this hospital on June 8. Physical examination revealed hypertension (170/90mmHg). On neurological examination, his consciousness was clear but he was demented. He showed disorientation, amnesia, and urinary incontinence. His most prominent symptom was disturbance of speech, including fluent aphasia and alexia with agraphia. Additionally, he showed ideomotor apraxia, construction apraxia, right-left agnosia, finger agnosia, and acalculia. On July 9, he had a transient attack of right hemiplegia with confusion. The brain CT scan performed on admission was unremarkable except for cavum septi pellucidum and a small low density area in the right basal ganglia. However, single photon emission computed tomography (SPECT) by 123I-labeled N-isopropyl-p-iodoamphetamine disclosed hypoperfusion of the cerebral blood flow in the border zones of the temporoparietal and frontal lobes on the left. A follow-up brain CT scan taken one month later demonstrated low density in the new areas corresponding to hypoperfusion shown by SPECT. Although the clinical features of the present case resembled those of DAT, dementia in this case was regarded as the result of multiple cerebral infarction since it occurred acutely with mild motor deficits, and brain CT scans and SPECT showed lesions indicating focal cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Multi-infarct dementia clinically simulating dementia of Alzheimer type. A comparison with angular gyrus syndrome]. 278 20

A 39 year old white man, with advanced Virchowian hanseniasis died with signs of extensive meningeal involvement. His medical background showed repeated episodes of Erythema nodosum hansenicum (ENH) in the last three years of his life, besides ischemic gangrena with amputation of the left leg and cerebral vascular ischemic attacks. The autopsy revealed an advanced stage of arteriosclerosis affecting mainly the brain and the distal segment of the aorta and its ramifications. A propagating thrombus was found along the left femoral and iliac arteries and in the terminal portion of the aorta extending to the renal arteries. Thrombosis was also found along the left femoral vein, left iliac vein and distal segment of the inferior cava. The brain showed anemic infarction in organization and a generalized meningoencephalic involvement with granulomatous reaction caused by Cryptococcus neoformans. It was suggested a possible relationship between Erythema nodosum reactions and thrombosis phenomena. Torulosis was considered as a final occurrence and the proliferative vasculitis due to the granulomatous process in the sub-arachnoidal space has certainly aggravated the cerebral ischemia.
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PMID:[Cryptococcus neoformans meningoencephalitis as a complication of arteriosclerotic vascular insufficiency in Virchowian leprosy]. 734 2

A 51-year-old male suffering from recurrent cerebral ischemia due to total occlusion of the bilateral intracranial vertebral arteries more than 1 month old was successfully treated by percutaneous transluminal angioplasty (PTA). The totally occluded portion from the right intracranial vertebral artery to the basilar artery was adequately dilated. Follow-up angiography approximately 3 months after angioplasty demonstrated no evidence of restenosis. His symptoms have not recurred. PTA is potentially a much less invasive and safer reconstruction than bypass surgery for total occlusions of the intracranial vertebral arteries less than 3 months old.
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PMID:Successful percutaneous transluminal angioplasty of the intracranial vertebral artery 1 month after total occlusion--case report. 752 43

We have examined the effect of cortical spreading depression (SD) and anoxic depolarization (AD) on the interstitial concentration changes of amino acids (AA) in the neocortex of anesthetized rats using microdialysis and HPLC. Accompanying SD alanine increased to 126 +/- 11%, arginine to 116 +/- 3%, aspartate to 160 +/- 17%, glutamate to 163 +/- 9%, glycine to 158 +/- 21%, serine to 125 +/- 9%, and taurine to 172 +/- 15% (mean +/- 1 S.E.M.). The increases lasted for about 1 min. Histidine decreased to 74% +/- 4% at 1 min following SD, and returned to normal 4 min later. Cardiac arrest triggered AD after approximately 2 min, immediately followed by changes of interstitial AAs. At 5 min after AD alanine had increased to 183 +/- 13%, aspartate to 3,458 +/- 656%, GABA to 338 +/- 35%, glutamate to 1,696 +/- 546%, glycine to 297 +/- 37%, serine to 153 +/- 12%, and taurine to 1721 +/- 98% as compared to control values (mean +/- 1 S.E.M.). Histidine decreased to 78 +/- 2% at 3 min following AD while arginine exhibited insignificant variations around the baseline. The increase of glutamate during SD is consistent with activation of NMDA-receptors as an essential requirement for this reaction. The increase of AAs may also contribute to the sequence of events leading to AD, though the exact mechanism remains unknown. SD is an important pathophysiological mechanism of the ischemic penumbra associated with focal cerebral ischemia, while AD reflects the electrophysiological status of the infarct core.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microdialysis of interstitial amino acids during spreading depression and anoxic depolarization in rat neocortex. 833 Feb 14

Histidine is an efficient scavenger of highly active singlet oxygen and somewhat weaker scavenger of hydroxyl radicals. And it has been shown to protect against reperfusion injury in the heart. The effects of L-histidine were examined in the forebrain ischemia reperfusion injury of the rat hippocampus (CA-1). Male Wistar rats were treated with the free radical scavenger L-histidine for 30 minutes before transient forebrain ischemia produced by 4-vessel occlusion. The extracellular concentrations of glutamate were measured by cerebral microdialysis. The intravenous (i.v.) administration of 50 mg/kg and 100 mg/kg L-histidine protected the elevation of extracellular glutamate concentrations after transient cerebral ischemia (p < 0.01). And the administration of L-histidine prevented ischemia-reperfusion induced delayed neuronal death in the rats. Morphological changes in the CA-1 sector of the hippocampus were evaluated 7 days after 10 minutes occlusion. The average neuronal density of treated groups showed a statistically significant (p < 0.01) persistence compared with that of control groups. These results indicate that L-histidine can reduce neuronal damage after reperfusion of cerebral ischemia and further suggest that excitatory amino acid and oxygen free radicals may damage the brain by a common pathway.
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PMID:[Protective effect of L-histidine (singlet oxygen scavenger) on transient forebrain ischemia in the rat]. 923 48

Involuntary episodic movements associated with transient cerebral ischemia are a rare but well-described presentation of carotid artery occlusive disease. We describe a young man with a left carotid artery occlusion who presented with daily episodes of involuntary movements of the right side that occurred for months. His symptoms virtually disappeared after his antihypertensive drug was reduced. This case supports the possibility of noninvasive management of this condition, which is traditionally treated with revascularization procedures.
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PMID:Limb-shaking carotid transient ischemic attacks successfully treated with modification of the antihypertensive regimen. 923 80

System-N transport plays an important role in l-glutamine uptake into isolated rat choroid plexus but its role in the transport of another System-N substrate, l-histidine, has yet to be determined. Similarly, the possible effects on System-N mediated l-histidine transport of changes in pH and extracellular l-glutamine, such as occur in cerebral ischemia and hepatic encephalopathy, have yet to be examined. In the absence of competing amino acids, l-[3H]histidine uptake in isolated rat choroid plexus was mediated by both Na+-independent and Na+-dependent transport. The former was inhibited by 2-amino-2-norbornane carboxlic acid, indicating System-L transport, while the latter appears System-N mediated as it was inhibited by three System-N substrates but not substrates for System-A and -ASC. The Na+-dependent uptake had a Km of 0.2 mM and a Vmax of 1.4 nmol/mg/min. It accounted for 30% of l-histidine uptake in the presence of physiological concentrations of amino acids. Reductions in pH markedly inhibited Na+-dependent but not Na+-independent transport indicating that, as in liver but not neurons, System-N mediated transport at the choroid plexus is pH sensitive. Increases in l-glutamine concentration in the pathophysiological range reduced l-histidine uptake via both System-L and -N.
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PMID:Choroid plexus histidine transport. 947 41

The purpose of this study was to evaluate whether the synthetic adrenocorticotropin-(4-9) (ACTH-(4-9)) analogue ORG 2766, HMet(O2)-Glu-His-Phe-D-Lys-Phe-OH, which has been shown to have beneficial effects on both the recovery from experimentally induced lesions of the central nervous system and peripheral nerve degeneration, has a protective effect on focal ischemic neuronal damage. The NMDA receptor antagonist dizolcipine (MK-801), a very potent neuroprotective drug, was used as positive reference compound. Isoflurane-anesthetized rats had the middle cerebral artery occluded using either an intravasal or an extravasal technique, because pilot experiments had shown differences in the severity of ischemia for the two middle cerebral artery occlusion techniques. MK-801, 500 microg kg(-1) min(-1), or saline was administered i.v. 30 min after occlusion of the middle cerebral artery. In the ACTH-(4-9) analogue/saline group, 10 and 150 microg/kg of the analogue, or saline was injected s.c. both directly after and 24 h after occlusion. The ACTH-(4-9) analogue treatment had no effect on the infarction volume in either model of middle cerebral artery occlusion, whereas MK-801 caused a significant reduction in the volume of cortical infarction in both models. We conclude that, although ORG 2766 is known to enhance the recovery from experimentally induced lesions of the central nervous system through a neurotrophic action and has proven to have significant beneficial effects on peripheral nerve regeneration, it did not prevent ischemic neuronal damage after intravasal or extravasal middle cerebral artery occlusion in rats. The results with MK-801, which caused significant reductions in the volume of cortical infarction in both models of middle cerebral artery occlusion, with clearly the largest reduction in the intravasal middle cerebral artery occlusion model, again indicate that there are differences in the severity of the cerebral ischemia which the two models produce in the rat brain.
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PMID:The effect of the adrenocorticotropin-(4-9) analogue, ORG 2766, and of dizolcipine (MK-801) on infarct volume in rat brain. 965 55

A 47-year-old man developed progressive muscular weakness in the left arm. MR images revealed low intensity signal lesions with ring enhancement by Gd-DTPA in right fronto-parietal lobes. At that time cerebral angiography was not performed because he refused. A tuberculin skin test showed strongly positive reaction and then administration of anti-tuberculous drugs was started. His symptom had remained stable for one year, but left facial palsy and dysarthria added about two years later. MR images revealed expansion of the lesions in right parietal lobe, adding cortical high intensity signal lesions with Gd-DTPA enhancement on T1-weighted images. Angiography disclosed tubular stenosis of right internal carotid artery at the portion of cervical to petrous segment and the local stenosis at right renal artery. These lesions were considered to be caused by fibromuscular dysplasia, but not atherosclerosis, because we could not find any atherosclerotic lesions in other arteries including right carotid bifurcation. His manifesting symptoms were ascribed to slowly progressive cerebral ischemia. And peculiar MRI findings in his early stage resembled those of inflammatory granulomatous diseases.
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PMID:[A peculiar MRI findings in a case with slowly progressive cerebral ischemia caused by internal carotid artery stenosis possibly due to fibromuscular dysplasia]. 1065 64


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