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)

We report on four patients with a histologically proven diagnosis of arteritis temporalis and clinical and/or neuroradiological evidence of severe focal cerebral ischemia due to intracranial vasculitis. While one patient suffered from a transient ischemic attack, CCT and MRI scans of the other patients showed multiple lacunar infarctions, combined with territorial infarctions in two cases. Necropsy in one patient demonstrated generalized giant cell vasculitis in large and small cerebral vessels. We suppose that the cerebral involvement was provoked by insufficient steroid therapy of arteritis temporalis in two patients. In one case, remission could be achieved by a combination of high-dose steroids and cyclophosphamide; one further patient remitted under lower steroid dosage. Steroid therapy was ineffective in two patients, one of whom died due to secondary complications. We conclude that central nervous system affection is a rare but dangerous complication of arteritis temporalis and may present as cerebral micro- and macroangiopathy.
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PMID:Temporal arteritis with cerebral complications: report of four cases. 803 43

We investigated the effect of KW-3635, a selective thromboxane (TX) A2-receptor antagonist, on the arachidonic acid (AA)-induced transient cerebral ischemia in anesthetized dogs. Intracarotid-arterial injection of AA (0.25-1 mg/kg) produced a transient and reversible decrease in electroencephalographic (EEG) activity. The reduction of EEG power was inhibited by the intravenous injection of KW-3635 or aspirin, a cyclooxygenase inhibitor. Local cortical perfusion (LCP) measured by a laser-doppler flow meter was also reduced concomitantly with the reduction of EEG power. Although KW-3635 at 1 and 3 mg/kg (i.v.) did not affect the maximum reduction of LCP, the duration of the reduction period of LCP was significantly shortened by KW-3635. On the other hand, aspirin at 1 and 3 mg/kg (i.v.) inhibited both the maximum and the delay of LCP reduction. The intravenous administration of KW-3635 or aspirin caused dose-dependent inhibition of ex vivo platelet aggregation stimulated by AA (150 microM) at the doses that improve the EEG activity. These data suggest that TXA2 is one of the important factors in the AA-induced transient reduction of EEG activity in anesthetized dogs. The TXA2-receptor antagonist may be useful for protection against the ischemic brain damage following transient ischemic attack.
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PMID:Protective effects of KW-3635, a thromboxane A2 antagonist, on arachidonic acid-induced transient cerebral ischemia in dogs. 808 29

We examined the alterations of opioid (naloxone), N-methyl-D-aspartate and gamma-aminobutyric acidA receptors in the gerbil brain 7 days after cerebral ischemia using [3H]naloxone, [3H]MK-801 and [3H]muscimol autoradiography, respectively. We also evaluated the effect of vinconate against the alterations in these receptors. Transient cerebral ischemia was induced for 10 minutes, and vinconate (100 and 300 mg/kg) was given intraperitoneally 10 minutes before ischemia. [3H]MK-801 binding showed a more severe reduction than [3H]naloxone binding 7 days after cerebral ischemia, whereas [3H]muscimol binding was unchanged in almost all brain regions. Vinconate showed a significant prevention against the reduction in [3H]naloxone binding in all brain areas. This drug also prevented a significant reduction in [3H]MK-801 binding in most of the brain regions. Furthermore, [3H]muscimol binding in vinconate-treated gerbils exhibited a significant increase compared with that in sham-operated animals. These results show that opioid and N-methyl-D-aspartate receptors are very sensitive to transient cerebral ischemia, whereas gamma-aminobutyric acidA receptors are particularly resistant. They also suggest that vinconate has a potent protective effect against the alterations of opioid and N-methyl-D-aspartate receptors. These findings might be of interest in relation to the mechanism of ischemic neuronal damage.
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PMID:Effect of vinconate against alterations in [3H]naloxone, [3H]MK-801 and [3H]muscimol bindings after transient cerebral ischemia in gerbils. 811 27

The relationship between the presence of silent cerebral infarcts (SCI) and etiology of an acute cerebral ischemia remains controversial. In a population of 306 patients with a first-ever stroke (225) or transient ischemic attack (TIA) (81), we studied the prevalence and associated risk factors of SCI as well as the presumed etiology of the qualifying event. Silent infarction was defined as a focal hypodensity on brain CT, not related to the recent ischemic event. The overall prevalence was 33% (102/306) with a higher rate in stroke patients (83/225, 37%) than in TIA patients (19/81, 23%; p = 0.028). Age (p < 0.01), smoking (p < 0.01), hypertension (p = 0.013), and leukoaraiosis (p = 0.05) were significantly associated with SCI, but only in some degree in TIA patients. Presence of SCI was statistically associated with a small-artery disease (p < 0.01) considered as the cause of the qualifying event. Emboligenic cardiopathy was significantly more frequent in patients without SCI (p < 0.05) in the TIA subgroup. Thus, in patients with silent cerebral infarcts, small-vessel disease may be in most cases the cause of the recent symptomatic cerebral ischemia.
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PMID:Stroke subtypes and risk factors associated with silent infarctions in patients with first-ever ischemic stroke or transient ischemic attack. 814 Aug 83

We investigated the postischemic alterations in dopamine D1 receptor and Ca2+/calmodulin independent cyclic adenosine monophosphate (cyclic AMP) selective phosphodiesterase in gerbils and examined the effect of pentobarbital on these alterations. [3H]SCH 23390 and [3H]rolipram, respectively, were used to label dopamine D1 receptor and Ca2+/calmodulin independent cyclic-AMP selective phosphodiesterase. Transient cerebral ischemia was induced for 10 min, and pentobarbital (40 mg/kg) was administered intraperitoneally 30 min prior to ischemia. 5 h after ischemia, [3H]rolipram binding decreased significantly in the striatum and hippocampus, whereas no significant change was found in [3H]SCH 23390 binding. 7 days after ischemia, however, there was a marked reduction in both [3H]SCH 23390 and [3H]rolipram binding in the striatum and hippocampus, where histological neuronal damage was found. Pentobarbital significantly ameliorated postischemic decreases in [3H]rolipram binding both 5 h and 7 days after recirculation in most areas studied. Furthermore, this drug significantly prevented postischemic reduction in [3H]SCH 23390 binding (only) 7 days after ischemia. These results suggest that alteration of cyclic AMP selective phosphodiesterase is more sensitive at an earlier stage after ischemic insult than that of dopamine D1 receptors. Our results also demonstrate that pentobarbital reduces the alteration in [3H]SCH 23390 and [3H]rolipram binding after cerebral ischemia.
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PMID:Effect of pentobarbital on postischemic SCH 23390 and rolipram binding in gerbil brain. 822 65

Because there is uncertainty about the role of atherogenic and nonatherogenic risk factors for cerebral ischemia in the young, we carried out a multicenter, hospital-based, case-control study. 333 patients (15-44 years) with focal cerebral ischemia (transient ischemic attack or stroke within 8 weeks of admission) were eligible. 25 patients were excluded, according to the protocol. 308 cases were matched by age and gender to one hospital and one population control. Independent risk was shown by logistic conditional regression for migraine with aura [odds ratio (OR) = 14.8], smoking (OR = 3.7), alcohol (OR = 2.8), serum triglycerides (OR = 1.6), arrhythmias (OR = 9.5), mitral stenosis (OR = 56), coronary heart disease (OR = 4.3) and carotid stenosis or occlusion (OR = 41). Serum HDL-cholesterol had a relative protective effect (OR = 0.8). These data confirm the role of atherosclerosis and cardiac diseases as well as migraine with aura and alcohol consumption in the pathophysiology of cerebral ischemia in the young. More thorough prevention programs may contribute to earlier detection and control of all of these risk factors, but further investigations in patients with as yet unidentified risk factors are warranted because the above-mentioned factors do not account for the total risk of ischemic stroke in the young.
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PMID:Focal cerebral ischemia in young adults: a collaborative case-control study. The National Research Council Study Group. 823 6

Transesophageal echocardiography (TEE) improves the diagnostic accuracy of transthoracic echocardiography in the identification of potential cardiac sources of embolus. However, there are few studies of the impact of TEE on the medical management of patients with focal cerebral ischemia. The records of 52 consecutive, hospitalized patients undergoing both TEE and transthoracic echocardiography for suspected cardiac source of embolus were reviewed to determine the influence of TEE on the decision to anticoagulate patients. Of 52 patients, 39 had focal cerebral ischemia (transient ischemic attack, n = 9; acute cerebral infarction, n = 30). In 4 of these 39 patients (10%), the TEE results changed the management of anticoagulation. In 19 of 39 patients (49%), the TEE results helped confirm anticoagulation decisions, and in 16 (41%), the results had no effect on anticoagulation decisions, because of overriding clinical information. Ten of the latter 16 patients had TEE evidence for a possible source of an embolus, but were not anticoagulated; 5 of these were poor candidates for long-term anticoagulation, and the others had right-to-left shunting across a patent foramen ovale or an interatrial septal aneurysm. Clinical variables (atrial fibrillation, TEE findings and pre-TEE anticoagulation status) were considered as possible predictors of post-TEE anticoagulation status using logistic regression analysis; the strongest predictor of post-TEE anticoagulation status was pre-TEE anticoagulation status (p < 0.0005). Despite the selection of patients presumed to receive maximal benefit from TEE, this study suggests that TEE findings are not predictive of subsequent anticoagulation management. However, TEE is at least confirmatory of anticoagulation decisions in most cases.
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PMID:Impact of transesophageal echocardiography on the anticoagulation management of patients admitted with focal cerebral ischemia. 824 49

Inductions of mRNAs for heat shock protein (HSP) 70 and heat shock cognate protein (HSC) 70 were examined in the cerebral cortex, cerebellum, heart, lung, kidney, and liver of gerbils after a 10-min transient forebrain ischemia. HSP70 mRNA was normally expressed in a small amount in the cerebellum, lung, and kidney, but was not expressed in the heart or liver in a detectable amount. A very small amount of HSP70 mRNA was also present in the cerebral cortex. HSC70 mRNA was normally present in all the organs examined with a variety in the amount. Eight hours after the cerebral ischemia, the level of HSP70 mRNA increased in the cerebral cortex, lung, and kidney. HSC70 mRNA levels also increased in all the organs. However, the increase of HSC70 mRNA was remarkable in the heart. Transient cerebral ischemia caused subsequent hyperthermia. Treatment of gerbils with an artificial hyperthermia without cerebral ischemia increased the HSP70 and HSC70 mRNA levels as well. However, the HSC70 mRNA level in the heart after cerebral ischemia was much higher than that in the case with hyperthermic treatment. These results suggest that HSC70 mRNA was preferentially induced in the heart after transient forebrain ischemia that was not only due to the subsequent hyperthermia.
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PMID:Preferential expression of HSC70 heat shock mRNA in gerbil heart after transient brain ischemia. 826 47

In 134 patients (age 41-74 years) with symptoms of a transient ischaemic attack the authors made an ultrasonic dopplerometric examination of the main arteries of the head and a rheoencephalographic examination using the method of polygraphic recording with an ECG tracing II. st. 1. as well as in extreme position of the head and neck. In the investigated group in seven subjects a severe disorder of the cardiac rhythm was recorded with more than one third of ectopic ventricular contractions. The authors elaborated criteria for the objective expression of the impact of haemodynamic changes on the cerebral circulation. When doing so, they took into account the number of inadequate ventricular contractions with a pulse deficit in the periphery, the frequency of inadequate contractions and their haemodynamic effect the consequence of which was reduction of the pulse volume and slowing down of the blood flow. According to these criteria dysrhythmia was the cause of cerebral ischaemia in 4.5% of all subjects included in the authors' group. In the group of patients with a severe disorder of the cardiac rhythm dysrhythmia was the cause of a transient ischaemic attack in 86% of the patients. Trespassing of the ischaemic threshold is promoted also by a poorer blood supply in extreme positions of the head and neck which may occur in everyday life or during sleep.
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PMID:[Hypoperfusion of the brain in cardiac rhythm disorders]. 829 41

This study was a prospective evaluation of the Durban experience with carotid endarterectomy over the past decade. Since 1981, 478 carotid endarterectomies have been performed in 411 patients. The majority of these patients were white men, with an average age of 60.6 years. The indication for surgery was a lateralising transient ischaemic attack or amaurosis fugax in 65.5%, lateralising stroke (< 1 year before surgery) in 14.4%, non-lateralising global cerebral ischaemia in 9.4% and asymptomatic carotid stenosis in 10.7%. Carotid endarterectomy was performed under general anaesthesia and with invasive monitoring; 25% of patients underwent selective shunting. After open carotid bifurcation endarterectomy, all but 6 underwent primary closure (99.4%). The combined major stroke/mortality rate was 6%. This audit identified a group of patients who presented with a history of stroke within the year preceding surgery and who had a significantly higher postoperative stroke/mortality rate of 20.2%. Long-term follow-up, ranging from 1 month to 96 months, showed 80.7% to be stroke-free after 8 years. This audit demonstrates a postoperative stroke/mortality rate comparable to that of other series and additionally confirmed the durability of carotid endarterectomy in the long term.
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PMID:Carotid endarterectomy in Durban--the first 10 years. 831 20


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