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)

Eight patients with common carotid artery (CCA) occlusion underwent bypass with saphenous vein to either the carotid bifurcation (five), the internal carotid artery (two), or the external carotid artery (one). Indications included ipsilateral transient ischemic attack (two), recent nondisabling hemispheric stroke (two), and transient nonhemispheric cerebral symptoms (two). Two asymptomatic patients with CCA occlusion and contralateral internal carotid stenosis underwent prophylactic revascularization prior to planned aortic surgery. There were no perioperative strokes, occlusions, or deaths. Late ipsilateral stroke occurred in two patients, and one patient had a single transient ischemic attack after 2 years. The four patients with preoperative transient cerebral ischemia experienced relief of their symptoms. Duplex ultrasound is an accurate screening modality for distal patency. Collateral filling of the internal or external carotid artery can usually be demonstrated after aortic arch or retrograde brachial contrast injection. End-to-end distal anastomosis after endarterectomy eliminates the original occlusive plaque as a potential source of emboli. The subclavian artery is preferred for inflow on the left. The CCA origin is easily accessible for inflow on the right. Bypass of the occluded CCA is safe and may be effective in relieving transient cerebral ischemic symptoms, although long-term ipsilateral neurologic sequelae may still occur.
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PMID:Surgical treatment of common carotid artery occlusion. 844 33

Even during the symptom-free stages, patients with a TIA often experience cerebral blood flow disturbances. In order to evaluate the factors which cause this abnormality, we studied the cerebral blood flow disturbance, anatomy and clinical status in 21 patients after TIAs. The results of 99mTc-hexamethyl-propylene-amine oxime SPECT were compared with CT, cerebral angiogram, cerebrovascular risk factors and clinical findings to determine which factor is most responsible for the hypoperfusion of brain after TIA. The overall sensitivity rates in detecting a lesion were 67% in SPECT and 19% in CT. The hypoperfused area tended to be large in patients who had intracranial, severe stenotic, multiple, or hemodynamically significant arterial lesions on the ipsilateral side. No such relationships were found between other examinations. We conclude that hypoperfusion after TIA essentially reflects a continuous cerebral blood flow disturbance that can be attributed to atherosclerosis of the cerebral arteries, with subsequent embolic and/or hemodynamic cerebral ischemia, although there may be a variety of processes.
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PMID:Factors causing prolonged hypoperfusion after transient ischemic attack. 846 Dec 36

Fifty patients of either sex with acute and chronic cerebrovascular disorders were submitted to an observation protocol and treated with oral nimodipine (tablets or drops) at a daily dosage of 90 mg for 1 to 3 months. Nimodipine proved useful both from the therapeutic point of view and for its easy handling in acute pathology (TIA, RIND, minor stroke, complete stroke) as well as chronic cerebral ischemia. The drug was well tolerated both locally and systemically; in patients with concomitant arterial hypertension, nimodipine reduced blood pressure with a tendency towards stabilization at near-normal levels.
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PMID:[Nimodipine in ischemic cerebropathy]. 847 25

The clinical records of patients withdrawn from the UK-TIA Aspirin Trial after identification of a brain tumour were reviewed. Certain features of transient focal neurological dysfunction were associated with an underlying brain tumour rather than transient ischaemia: a) focal jerking or shaking; b) pure sensory phenomena; c) loss of consciousness; d) isolated aphasia or speech arrest. In several patients the misdiagnosis occurred because these features were interpreted as the sequelae of previous ischaemic damage. When a transient focal neurological attack is associated with any of these features, a brain tumour must be considered. If patients later develop epilepsy the diagnosis of cerebral ischaemia should be reviewed.
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PMID:Intracranial tumours that mimic transient cerebral ischaemia: lessons from a large multicentre trial. The UK TIA Study Group. 850 52

The main symptoms of stroke such as a displacement of intracranial structures, changes in spatial relations, secondary hemorrhagic and ischemic foci, oedema and metabolic disturbances are the cause of the disorders of hypothalamus-hypophysis system leading to increased secretion of corticosteroids including 17-hydroxyketosteroids (17-OHKS). Steroidogenesis in inhibited by high concentrations of ascorbic acid. Intravenous injections of ascorbic acid 0.5 g were given to the patients with stroke and their urine was analysed daily to examine the secretion of 17-OHKS. A slight increase in 17-OHKS secretion was found on 1 and 2 days of the disease in patients suffering from TIA and a significant increase in 17-OHKS secretion was detected in patients with cerebral ischaemia (ischemic stroke) and cerebral hemorrhage and persisted for 3-4 days of the illness. One can presume that the disorders of hypothalamus-hypophysis-adrenal system contributes much more to the decrease in 17 OHKS secretion on successive days of stroke than the administration of ascorbic acid.
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PMID:[The effect of intravenous ascorbic acid on urinary 17-hydroxysteroid excretion at an early stage of cerebral stroke]. 865 50

Transient cerebral ischemia induces, besides delayed neurodegeneration in selected brain structures, a number of early responses which may mediate ischemic injury/repair processes. Here we report that 5 min exposure to cerebral ischemia in gerbils induces a rapid inhibition and subsequent translocation of Ca2+/calmodulin-dependent protein kinase II (CaMKII). These changes were partially reversible during a 24 h post-ischemic recovery. Concomitantly the total amount of the enzyme protein, as revealed by Western blotting (alpha-subunit specific), remained stable. This is consistent with our previous hypothesis, that the mechanism of ischemic CaMKII down-regulation involves a reversible posttranslational modification-(auto)phosphorylation, rather than the degradation of enzyme protein. The effectiveness of known modulators of post-ischemic outcome in counteracting CaMKII inhibition was tested. Three of these drugs, namely dizocilpine (MK-801), N-nitro-L-arginine methyl ester (L-NAME) and ginkgolide (BN52021), all significantly attenuated the enzyme response to ischemia, whereas an obvious diversity in the time-course of their actions implicates different mechanisms involved.
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PMID:Changes of Ca2+/calmodulin-dependent protein kinase-II after transient ischemia in gerbil hippocampus. 878 2

Transient cerebral ischemia in fetal sheep is followed by a period of delayed cerebral injury associated with cerebral vasodilation. As nitric oxide (NO) can mediate both vasodilation and neuronal death, this study investigated whether inhibition of NO synthesis would attenuate the vasodilation and decrease cerebral injury. Eleven late gestation (range 122-133 d) fetal sheep were subjected to 30 min of transient cerebral ischemia in utero. Two hours later, treatment group (n = 5) received a continuous infusion of NG-nitro-L-arginine (L-NNA) at a dose of 50 mg.h-1 for 4 h followed by 20 mg.h-1 for the subsequent study period, a competitive inhibitor of NO synthase (NOS), whereas a control group (n = 6) received PBS. Inhibition of NOS activity was confirmed in the treatment group by 1) suppression of the fall in mean arterial blood pressure (MAP) associated with acetylcholine (p < 0.01), and 2) persistent increase in MAP after commencement of L-NNA (p < 0.05). Changes in cerebral blood volume (CBV) were observed for 3 d by measuring changes in concentration of total cerebral Hb ([tHb]) using near infrared spectroscopy. The delayed increase in CBV commenced at 13.1 +/- 1.0 h postischemia in the control and 12.7 +/- 2.3 h in the treatment group. Maximum increase at 30-36 h was 0.5 +/- 0.1 mL.100 g-1 in the treatment group and 1.2 +/- 0.2 mL.100 g-1 in the control (p < 0.05). Final CBV was depressed below preischemic baseline in the treatment (-0.7 +/- 0.2 mL.100 g-1) but not the control group (-0.1 +/- 0.3 mL.100 g-1) (p < 0.05). Neuronal loss, quantified histologically 3 d postischemia, indicated that cerebral injury was increased in the treatment group (p < 0.05). The results indicate that after transient cerebral ischemia in fetal sheep, NOS inhibition attenuates the delayed rise in CBV but does not decrease the extent of cerebral injury.
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PMID:Nitric oxide synthase inhibition attenuates delayed vasodilation and increases injury after cerebral ischemia in fetal sheep. 882 65

The mechanisms of ischemic cell damage are still not fully understood. It has been shown that alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionate (AMPA)/kainate receptor antagonists, such as 6-nitro-7- sulphamoyl-benzo-(f)-quinoxaline-2, 3-dione (NBQX), are neuroprotective in models of transient forebrain ischemia, even when applied during recovery, indicating that nonNMDA receptors may play a pivotal role in ischemic cell damage. In the present series of experiments, we studied whether transient cerebral ischemia causes changes in the extent of mRNA editing of AMPA/kainate receptor subunits, a reaction critical for the control of calcium flux through nonNMDA receptor ion channels. Transient cerebral ischemia was produced in rats using the four-vessel occlusion (4-VO) model. After 30 min of ischemia, brains were recirculated for 4, 8, or 24 h. Total RNA was extracted from the cortex, striatum, and hippocampus in order to analyze the extent of mRNA editing of the glutamate receptor subunits GluR2, GluR5, and GluR6. RNA was converted by reverse transcription into cDNA, which was used as a template for subunit-specific polymerase chain reaction (PCR) to amplify a product across the edited base A (A edited to I in the second transmembrane-spanning regions of GluR2, GluR5, and GluR6). PCR products were analyzed with the restriction enzyme Bbv 1, which recognizes the cDNA sequence GCAGC originating from unedited but not that originating from edited GluR2, GluR5, or GluR6 mRNA (GCGGC, the base I is read as G). Restriction digests were electrophoresed, and the bands visualized with ethidium bromide and then photographed. The extent of mRNA editing of the different subunits was quantified using image analysis and appropriate standards. In all control brains studied, GluR2 mRNA was completely edited and remained so after reversible cerebral ischemia. The extent of GluR5 mRNA editing was significantly upregulated in the striatum (from 39 +/- 6% in controls to 57 +/- 9 and 56 +/- 7 after 4 and 8 h of recovery, respectively, p < 0.05 versus control) but not in the cortex and hippocampus. The extent of GluR6 mRNA editing was significantly reduced after 24 h of recovery: in the cortex, from 92 +/- 1 to 78 +/- 6% (p < 0.01); in the striatum, from 91 +/- 2 to 79 +/- 1% (p < 0.001); and in the hippocampus, from 90 +/- 3 to 80 +/- 2% (p < 0.05). A significant reduction was already apparent in the striatum after 4 h of recovery (p < 0.05). Results indicate that mRNA editing is regulated differently in each of the glutamate receptor subunits GluR2, GluR5, and GluR6 after transient cerebral ischemia. The ischemia-induced upregulation of GluR5 mRNA editing observed in the striatum may be indicative of a higher sensitivity to transient ischemia of neurons that exhibit a large fraction of unedited GluR5 mRNA. This assumption is corroborated by the observation (Mackler and Eberwine, 1993) that GluR5 mRNA is completely unedited in neurons of the hippocampal CA1-subfield, a region most vulnerable to transient cerebral ischemia. Whether the decrease in GluR6 mRNA editing observed in all brain structures after ischemia results from a disturbance of the editing reaction or from glial proliferation will have to be established in further experiments. Studying ischemia-induced changes in mRNA editing of glutamate receptor subunits GluR5 and GluR6 may help to elucidate the molecular mechanisms of ischemic cell damage.
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PMID:RNA editing of glutamate receptor subunits GluR2, GluR5 and GluR6 in transient cerebral ischemia in the rat. 896 93

Patients who have sustained a preoperative stroke are at increased risk for perioperative stroke after carotid endarterectomy. At our institution this risk was recently shown to be increased two-to threefold. The purpose of this study was to investigate the reasons for the increased surgical risk in these patients. Records of 606 patients undergoing 704 consecutive carotid endarterectomies from 1988 through 1993 were reviewed. Patients who suffered preoperative strokes (n = 183) were compared to those who were either asymptomatic or experienced only transient ischemic attacks (TIAs) preoperatively (n = 423). Of the 183 patients who had suffered preoperative strokes, eight patients who experienced perioperative strokes after endarterectomy were compared with 175 who successfully underwent surgery. Patients with a prior stroke had an increased perioperative stroke rate (4.4% versus 1.2%, p = 0.01). They had a significantly higher incidence of hypertension (62.6% versus 47.9%, p < 0.001), cardiac disease (54.7% versus 40.7%, p = 0.001), and positive smoking history (52% versus 40.6%, p = 0.01) than did the asymptomatic/TIA patients. The presence of contralateral total occlusion was also significantly increased (22% versus 10.3%, p < 0.001). Although not statistically significant due to the overall small number of patients who sustained perioperative strokes, the preoperative stroke patients who sustained perioperative strokes had a higher incidence of hypertension (87.5% versus 61.5%) and contralateral total occlusion (37.5% versus 21.3%) than did those who successfully underwent surgery. Patients with both a prior stroke and contralateral total occlusion had a 7.5% perioperative stroke rate. Patients with both a prior stroke and hypertension had a 6.1% perioperative stroke rate. The perioperative strokes in patients with prior strokes were not related to the severity of the prior stroke, the interval between the stroke and surgery, the use of a shunt, or the type of anesthesia employed. Patients who have sustained preoperative strokes have a higher incidence of significant medical illnesses and overall cerebrovascular disease. Hypertension and total occlusion of the contralateral carotid artery appear to be particularly poor prognostic indicators of outcome after endarterectomy in these patients. Patients who have sustained preoperative strokes may be more likely to display clinical neurologic symptoms in response to any form of cerebral ischemia. In this higher risk subgroup, intraoperative and surgeon-dependent factors appear to play less of a role.
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PMID:Causes of the increased stroke rate after carotid endarterectomy in patients with previous strokes. 906 Nov 36

Two treatments, based on either ticlopidine or indobufen at their optimal individual daily dose (median dose: 250 and 200 mg/day, respectively), were compared in an open randomized multicenter trial in patients at risk of cerebral ischemia (men and women, aged 39 to 80 years, who had experienced in the month before entry into the study transient ischemic attack or amaurosis fugax or minor stroke). The total number of patients screened was 4033; 1632 were enrolled, 821 randomized to ticlopidine, 811 to indobufen. The overall frequency of the composite primary end-point (stroke, myocardial infarction, and death from any cause) was 4.4%. The ticlopidine-based regimen proved significantly better than the indobufen one in preventing the composite of fatal and non fatal events (49.6% relative risk reduction), or death alone (54.4% relative risk reduction). The two groups had similar percentages of adverse events (5.5% and 6.4% for ticlopidine and indobufen group, respectively) with withdrawals because of adverse events in 3.4% and 2.5%; gastrointestinal disorders and bleeding were more frequent in the indobufen group, whereas rash and abnormal liver function were more frequent in the ticlopidine one.
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PMID:A randomized trial comparing ticlopidine hydrochloride with indobufen for the prevention of stroke in high-risk patients (TISS Study). Ticlopidine Indobufen Stroke Study. 912 22


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