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

Purpose of this study was to define a subgroup of TIA/stroke patients who should be examined by transthoracal and transesophageal echocardiography or Holter-electrocardiography to identify those with cardiogenic brain embolism reliably; 300 consecutive patients with acute focal brain ischemia underwent a standardized diagnostic protocol for the evaluation of the etiology including, clinical examination by a cardiologist and routine electrocardiography, Holter-electrocardiography, transthoracal and transesophageal echocardiography. 188 patients had a potential cardiac source of embolism. In particular echocardiography was diagnostic in 163 patients, and Holter-electrocardiography 10; 159 of these 188 patients (84.6%) had competitive etiologies, predominantly large vessel atherosclerosis. In 136 patients cardiogenic brain embolism was assumed as quite definite or possible. To identify these patients reliably, transthoracal and transesophageal echocardiography would have been necessary in 89% of the entire group of patients (all with clinically cardiological abnormalities, pathological routine ECG, without vascular risk factors, or no atherosclerosis in duplex sonography), and Holter-electrocardiography in 54%.
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PMID:Specific cardiological evaluation after focal cerebral ischemia. 873 42

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

Neurons are so vulnerable to ischemic insults that transient forebrain ischemia for 5 min killed most CA1 neurons in the gerbil hippocampus (surviving neurons: 4%). In contrast, 2 days after a nonlethal challenge of 2-min ischemia, 51% of CA1 neurons became resistant to subsequent, otherwise lethal ischemia for 5 min. Bifemelane hydrochloride (20 mg/kg, i.p.), which helps ischemic brain recover from oxidative stress and inhibition of protein synthesis, significantly enhanced the 'ischemic tolerance' phenomenon if injected 1 day after 2-min ischemia: 94% of neurons survived after 5-min ischemia. This finding carries implications for possible preventive treatment following warning signs of transient ischemic attack.
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PMID:Bifemelane hydrochloride enhances 'ischemic tolerance' phenomenon in gerbil hippocampal CA1 neurons. 880 11

Clinically significant arterial occlusive disease developed in 26 patients at between 5 months and 44 years (mean(s.d.) 10.7(12.0) years) following radiation therapy. Therapeutic radiation was associated with lesions of the carotid artery (nine patients), subclavian-axillary arteries (seven) and the abdominal aorta and its branches (10). Clinical presentations included transient ischemic attack, stroke, vertebrobasilar insufficiency, carotid bruit, upper- or lower-extremity ischemia and renovascular hypertension. Surgery for cerebrovascular insufficiency included carotid endarterectomy with vein patch, interposition grafting or subclavian-to-carotid bypass. Carotid or subclavian-to-axillary bypass was performed for upper-extremity ischemia. A combination of endarterectomy and Dacron or saphenous vein grafts was used for infrarenal reconstruction. Tunnels were placed orthotopically. Musculocutaneous flaps assisted in healing selected wounds. Ureteral catheters were useful adjuncts in abdominal vascular reconstructions. There were no operative deaths, strokes or amputations. One patient had recurrent transient ischemic attacks following subclavian-to-carotid bypass. The mean(s.d.) postoperative follow-up was 48.1(39.6) months. Patients presenting with end-organ ischemia following radiation therapy can be managed successfully with aggressive surgical revascularization using a broad spectrum of reconstructive techniques.
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PMID:Management of arterial occlusive disease following radiation therapy. 886 26

Transient cerebral ischemia was produced in rats using the four-vessel occlusion model. After 30 min ischemia and 2, 4, 8, or 24 h of recirculation, total RNA was isolated from the cortex, striatum and hippocampus and reverse transcribed into cDNA. Endoplasmic reticulum (ER) calcium-ATPase (SERCA, subunit 2b) cDNA was amplified using appropriate primers. Ischemia-induced changes in SERCA mRNA levels were analyzed by quantitative polymerase chain reaction (PCR). For quantification, each PCR reaction was run in the presence of an internal standard. In control brains SERCA mRNA levels amounted to 392 +/- 43,431 +/- 86, and 409 +/- 21 micrograms mRNA/g total RNA in the cortex, striatum and hippocampus, respectively. SERCA mRNA levels did not change significantly during the first 8 h of recovery. After 24 h of recovery, however, SERCA mRNA levels decreased sharply in the hippocampus and striatum (P < 0.001 versus control) but not in the cortex. It is concluded that in vulnerable brain structures a post-ischemic disturbance in ER calcium homeostasis may limit the recovery of neurons from metabolic stress.
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PMID:Changes in endoplasmic reticulum Ca(2-)-ATPase mRNA levels in transient cerebral ischemia of rat: a quantitative polymerase chain reaction study. 890 35

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

This study was performed to investigate the role of leukocyte accumulation in human cerebral infarction and its association with neurological functional outcome. A total of 42 patients diagnosed as acute ischemic stroke (22 embolism, 17 thrombosis, 3 TIA) were examined. Leukocyte accumulation was studied using indium-111-labeled leukocyte brain single-photon emission computed tomography (SPECT). Volume of brain infarction was evaluated by CT and/or MRI. The data were compared with the cerebral blood flow (CBF) imaging. Immediately after CBF study by SPECT using either technetium-99m hexamethylpropyleneamine oxine (Tc-99m-HMPAO) or technetium-99m ethyl-cysteinate dimer (ECD), In-111-labeled autologous leukocytes were injected intravenously. Brain scan for leukocytes was performed after 48 hours. The European Stroke Scale was used for neurological assessment. Thirteen patients with cerebral embolism and three patients with cerebral thrombosis showed intensive accumulation of leukocytes in the region of low flow. Leukocyte's accumulation was not seen in patients with TIA. The accumulation of leukocytes was more noticeable in the central zone of the ischemia. Patients who showed negative leukocyte accumulation revealed clinically mild functional outcome and the size of infarction on CT and/or MRI was small. The regional accumulation of leukocytes was seen in all the patients with hemorrhagic infarction, but the degree of hemorrhage on CT did not have significant influence on the amount of leukocyte accumulation. Abnormal accumulation of leukocytes was associated with reduced CBF during the acute embolic stroke. The present clinical study revealed that leukocyte accumulation correlated with the poor neurological functional outcome in patients with acute embolic stroke. The present study confirms that leukocytes contribute to the ischemic tissue damage of the brain and demonstrates a clinical evidence that the regional accumulation of leukocytes has a deleterious effect on the brain following ischemia.
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PMID:[In-111-labeled leukocyte brain SPECT imaging in acute ischemic stroke in man]. 914 67

Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of experiments. In a primate model of SAH, serial ET-1 levels were measured in samples from the perivascular space by using a microdialysis technique and in cerebrospinal fluid (CSF) and plasma during the development and resolution of delayed vasospasm. To determine whether elevated ET-1 production was a direct cause of vasospasm or acted secondary to ischemia, the authors also measured ET-1 levels in plasma and CSF after transient cerebral ischemia. To elucidate the source of ET-1, they measured its production in cultures of endothelial cells and astrocytes exposed to oxyhemoglobin (10 microM), methemoglobin (10 microM), or hypoxia (11% oxygen). There was no correlation between the perivascular levels of ET-1 and the development of vasospasm or its resolution. Cerebrospinal fluid and plasma levels of ET-1 were not affected by vasospasm (CSF ET-1 levels were 9.3 +/- 2.2 pg/ml and ET-1 plasma levels were 1.2 +/- 0.6 pg/ml) before SAH and remained unchanged when vasospasm developed (7.1 +/- 1.7 pg/ml in CSF and 2.7 +/- 1.5 pg/ml in plasma). Transient cerebral ischemia evoked an increase of ET-1 levels in CSF (1 +/- 0.4 pg/ml at the occlusion vs. 3.1 +/- 0.6 pg/ml 4 hours after reperfusion; p < 0.05), which returned to normal (0.7 +/- 0.3 pg/ml) after 24 hours. Endothelial cells and astrocytes in culture showed inhibition of ET-1 production 6 hours after exposure to hemoglobins. Hypoxia inhibited ET-1 release by endothelial cells at 24 hours (6.4 +/- 0.8 pg/ml vs. 0.1 +/- 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05) and at 48 hours (6.4 +/- 0.6 pg/ml vs. 0 +/- 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05), but in astrocytes hypoxia induced an increase of ET-1 at 6 hours (1.5 +/- 0.6 vs. 6.4 +/- 1.1 pg/ml, control vs. hypoxic astrocytes; p < 0.05). Endothelin-1 is released from astrocytes, but not endothelial cells, during hypoxia and is released from the brain after transient ischemia. There is no relationship between ET-1 and vasospasm in vivo or between ET-1 and oxyhemoglobin, a putative agent of vasospasm, in vitro. The increase in ET-1 levels in CSF after SAH from a ruptured intracranial aneurysm appears to be the result of cerebral ischemia rather than reflecting the cause of cerebral vasospasm.
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PMID:Source and cause of endothelin-1 release into cerebrospinal fluid after subarachnoid hemorrhage. 925 95

Transient cerebral ischemia causes extensive cell death in hippocampal CA1 pyramidal cells and selective loss of interneurons in the dentate hilus. Many hippocampal interneurons can be classified by their contents of somatostatin (SS) and/or neuropeptide Y (NPY). Following ischemia in the rat, most of the NPY immunoreactivity is permanently lost in hippocampus. Furthermore, SS interneurons in the dentate hilus die, whereas CA1 interneurons survive and their expression of SS mRNA and peptide returns to preischemic levels within 16 days after ischemia. We have addressed the following questions: (1) Does the loss of NPY involve a specific downregulation in surviving CA1 interneurons that pre-ischemically expressed both SS and NPY? (2) Can the subpopulation of dying interneurons in hilus be identified from their preischemic coexpression of SS and NPY? We investigated the coexpression of SS mRNA and NPY peptide using combined in situ hybridization and immunocytochemistry. Cells containing one or both markers were counted in control sections and sections taken 2-16 days after ischemia from the hippocampal formation. In CA1, a decrease in the number of neurons containing NPY alone as well as a decrease in the number of neurons coexpressing NPY and SS was observed, whereas the number of neurons containing SS alone increased 16 days after ischemia. We conclude that neurons coexpressing SS and NPY before ischemia added to the number of neurons containing SS alone after ischemia, because NPY expression was selectively down regulated in the coexpressing population. In hilus, we demonstrated both survival and ischemic cell death of neurons expressing either SS, NPY or both, indicating that hilar interneurons dying from ischemia cannot unequivocally be identified from their preischemic colocalization of SS and NPY.
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PMID:Ischemia changes the coexpression of somatostatin and neuropeptide Y in hippocampal interneurons. 926 97

From 1981 to 1995 a total of 14 patients with a mean age of 52 years (range: 23-71) underwent surgery for 15 aneurysms of the extracranial internal carotid artery. Fusiform aneurysms of the carotid bifurcation were not included in this study. Aneurysm led to brain ischemia in 10 cases and rupture in one case. In the remaining four cases, aneurysm was asymptomatic including three that were detected following hemispheric stroke related to a contralateral aneurysm. The etiology was spontaneous dissection in four cases, blunt trauma in three cases, fibromuscular disease in five cases, and atheroma in three cases. The upper limit of the aneurysm was located at C1-C2 in six cases, at C1 in three cases, and above C1 (at the base of the skull) in six cases. The cervical approach was used to successfully perform 12 revascularizations and three ligations (including one after extra-intracranial bypass). There were no postoperative deaths. One transient ischemic attack (TIA) occurred after ligation. Peripheral facial paralysis (PFP) occurred in four of the nine cases in which an extended cervical approach was used. No patients were lost to follow-up. Mean duration of follow-up was 4 years (range: 2 months-10 years). Two patients died at 2 and 4 years of causes unrelated to the procedure. All carotid reconstructions are currently patent and no neurologic manifestations have occurred. PFP persisted in one case. The results of this series confirm that surgical therapy of aneurysms of the extracranial internal carotid artery achieves satisfactory short- and medium-term results and that the extended cervical approach allows treatment of lesions near the base of the skull.
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PMID:Results of surgical management of internal carotid artery aneurysm by the cervical approach. 930 60


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