Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the postischemic alterations in [3H]MK-801, [3H]muscimol, and [3H]naloxone binding in the gerbil brain, and examined the effect of pentobarbital against these alterations. [3H]MK-801, [3H]muscimol, and [3H]naloxone were used to label N-methyl-D-aspartate (NMDA), gamma-aminobutyric acidA (GABAA), and opiate receptors, respectively. Transient cerebral ischemia was induced for 10 min, and pentobarbital (40 mg/kg) was administered intraperitoneally 30 min before ischemia. Five hours after ischemia, no conspicuous alteration in [3H]MK-801, [3H]muscimol, and [3H]naloxone binding was found in the striatum and hippocampus. Seven days after ischemia, [3H]MK-801 and [3H]naloxone binding was significantly decreased in the striatum and hippocampal area where histological neuronal damage was noted. By contrast, no significant change in [3H]muscimol binding was seen in the above regions except for the hippocampal CA3 sector. The treatment of pentobarbital caused a significant alteration in the binding of [3H]naloxone and [3H]muscimol in various brain areas 5 h after ischemia. However, this drug showed no significant change in [3H]MK-801 binding in the brain. Seven days after ischemia, pentobarbital partly ameliorated a significant reduction in [3H]MK-801 and [3H]naloxone binding in the striatum and hippocampus. A histological study also showed that pentobarbital afforded neuronal protection against the damage to the brain except for the hippocampal CA1 sector 7 days after ischemia. These results suggest that NMDA and opiate receptors are damaged after ischemia, whereas GABAA receptors are unaffected. They also demonstrate that opiate receptors are severe affected by the treatment of pentobarbital, compared with NMDA and GABAA receptors. These findings are of interest in relation to the mechanism of ischemic neuronal damage.
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PMID:Effect of pentobarbital on postischemic MK-801, muscimol, and naloxone bindings in the gerbil brain. 782 Jun 43

From 1982 to 1992, 25 patients with subclavian steal syndrome (SSS) were admitted with 20 undergoing surgery. Etiology included atherosclerosis 56% (14/25), Takayasu's disease 36% (9/25), 14 of them were smokers. Stenosis or occlusion of the left subclavian artery were found in 14, the right in 7, and bilateral in 4. 14 cases had vertigo symptoms, 24 cases had claudication of the arm, 9 of them complained transient ischemic attack (TIA). Carotid to subclavian bypass were performed for 15 cases. Two patients underwent axilloaxillary bypass with evidence of both clinical and laboratory improvement. Aorta-Carotid graft bypass was done in 2 cases with good result in one. PTA was done for a girl with innominate severe stenosis but symptom recurred three months later. Symptoms of the upper extremity ischemia were relieved in 75% of the patients, and of the cerebrovascular ischemia in 50%. Our conclusion is that surgical therapy remains the treatment of choice in symptomatic patients.
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PMID:[Subclavian steal syndrome: a report of 25 cases]. 784 5

The role of the surface characteristics of carotid artery lesions in the long-term prognosis of cerebrovascular disease has not been established. 184 patients who presented with symptoms of hemispheric TIA or retinal ischemia, and had ipsilateral carotid artery atheromatous disease, were clinically followed 5-8 years (mean 6.3 years) after initial presentation. Based on the findings of the initial duplex ultrasound examination, a comparison was made between those patients who suffered a vascular event in the follow-up period and those who remained alive and without subsequent vascular symptoms. The only significant difference found between the groups was the distribution of the lesion surface characteristics (p < 0.01). The degree of stenosis caused by the lesion or the size of the low-echo pool within the lesion were not found to be significantly associated with subsequent clinical events. The results of this study emphasise the importance of the ultrasound evaluation of the carotid lesion surface characteristics, and their inclusion in the criteria for decisions on patient treatment.
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PMID:Prognostic value of ultrasound morphology in carotid atherosclerosis. 791 98

Establishing the cause of a transient ischemic attack (TIA) or minor stroke enables you to institute effective therapy to prevent major stroke. Clinical and radiologic features that help to clarify the cause of cerebrovascular ischemia include characteristics of prior TIAs, temporal progression and nature of the neurologic deficit, and appearance of infarction on CT and MRI of the brain. Carotid and transcranial Doppler ultrasound, magnetic resonance angiography, arterial angiography, and echocardiography are used to confirm the cause of cerebral ischemia. We provide three case studies to illustrate our approach to stroke diagnosis.
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PMID:Ischemic stroke and TIA: clinical clues to common causes. 791 76

Amaurosis fugax has been grouped together with other forms of transient ischemic attacks (TIAs) in the neurologic literature in analyses of prognosis. Although episodes of transient visual loss (TVL) are presumed to be due to ischemia, the prognosis with respect to subsequent stroke and myocardial infarct (MI) appears to differ from cerebral TIAs. We reviewed the clinical course of 73 patients above the age of 45 years who presented to our clinics with a distinct history of TVL. With an average follow-up period of 38 months, the incidence rates of cerebrovascular accident, cerebral TIA and MI following presentation with TVL were 1%, 4% and 7% respectively. Although there was a trend toward fewer episodes of amaurosis with use of acetylsalicylic acid (ASA), the difference was not statistically significant. In addition, ASA did not appear to offer a benefit with respect to future ischemic events. Patients with monocular TVL appeared more likely to experience a TIA, whereas those with binocular TVL appeared more likely to experience an MI.
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PMID:Amaurosis fugax: prognosis and the role of acetylsalicylic acid. 792 49

The frequency of silent infarction is an important issue because it is a marker of vascular disease. We studied the occurrence of silent infarction in a sample of patients from the Dutch TIA trial, in which patients were randomized between 30 and 283 mg of aspirin. A total of 91 patients with TIA or non-disabling ischemic stroke and who did not suffer a stroke during a period of one to four years (mean 32 months) underwent CT scanning both on entry and at the end of the study. A cardiac source of embolism was an exclusion criterion for the trial. We found only one patient with a possibly silent infarction; in four patients a previously detected symptomatic infarct on CT was no longer visible. The rarity of silent infarction in this study may have several explanations; (1) the relatively short period of follow-up, (2) the selection of patients (no cardiac source of embolism), (3) the clinical monitoring at four monthly intervals aimed at detection of focal ischemia, (4) the use of aspirin. Given these circumstances, silent infarction is an infrequent problem.
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PMID:Silent infarction on a second CT scan in 91 patients without manifest stroke in the Dutch TIA trial. 798 89

Venous angioma is a relatively rare vascular malformation of the brain. It is usually asymptomatic and may be an incidental finding at autopsy or on cerebral angiography. We report a very rare case in which TIA-like attack occurred as the initial manifestation. A 59-year-old woman was hospitalized because of a TIA-like attack about 5 months after left putaminal bleeding. Detailed examination allowed us to make a diagnosis of subcortical venous angioma of the left parietal lobe and multiple cerebral aneurysms. The cerebral aneurysms were treated surgically. Since the angioma was localized in an eloquent area, radiotherapy was chosen first. Angioma giving rise to TIAs is very rare. The ischemia may have been caused by transient venous thrombosis or a steal phenomenon due to a decrease in blood circulation in the left cerebrum caused by the putaminal bleeding.
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PMID:[A case of venous angioma complicated by unruptured aneurysm with TIA as the initial manifestation]. 806 42

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

Functional neuroimaging techniques such as positron and single-photon emission computed tomography (PET and SPECT) have contributed to our knowledge of pathophysiological changes in ischemic stroke. Determinations of cerebral blood flow (CBF), cerebral blood volume (CBV), and cerebral metabolic rate of oxygen (CMRO2) permit the discrimination of various compensatory mechanisms in occlusive vascular disease, where changes in the CBF/CBV ratio indicate a perfusional reserve and increases in the oxygen extraction fraction (OEF), a metabolic reserve, that prevent ischemic tissue damage during graded flow decreases. Early in the course of acute ischemia, CBF and CMRO2 below a certain threshold (approximately 12 ml/100 g/min and/or 65 mumol/100 g/min, respectively) indicate irreversible tissue damage, while preservation of CMRO2 with decreased flow resulting in increased OEF ("misery perfusion") suggests still viable tissue up to 48 h after the attack, which, however, turns into necrosis in most instances during the following period. In a few instances such tissues can survive, suggesting a potential for effective therapy. Transient ischemic attacks are caused by less severe regional flow disturbances and the consequent metabolic changes are not so significant. In these cases the impact of obstructive vascular changes on hemodynamic reserve can be evaluated by functional tests applying CO2 or acetazolamide. While the regional cerebral metabolic rate of glucose (rCMRglu) in early ischemia is often not coupled to flow or CMRO2 and might even be increased (nonoxidative glycolysis with consequent tissue lactacidosis), this variable is the best indicator of permanent impairment of tissue function. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of PET and SPECT in the assessment of ischemic cerebrovascular disease. 811 May 93

The concept of vascular origin in vertigo and equilibrium disorders is only a pragmatic clinical tool used to initiate and direct complex, complementary clinical investigation to determine the location (peripheral, central or mixed), the pathophysiological mechanisms and the multiple etiologies of the vestibular disorder. The concept includes focal and systemic ischemic processes and haemorrhagic processes of the posterior fossa. If the vertigo is associated with central neurological signs, the method can lead to certain diagnosis. If such signs are not detected by neurological screening of all the intra-axial signs of the vertebrobasilar regions, the diagnosis is uncertain clinical. Screening associated CT scan and MRI is more reliable than neuro-otological quantification. The major diagnostic difficulty involves TIA. Vertebrobasilar appears to be more heterogeneous than carotid ischemia. Schematic distinction is possible to differentiate thrombo-embolic from hemodynamic TIA. It is based on methodic clinical analysis and complementary investigations that are of unequal value.
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PMID:[Vertigo of vascular origin]. 817 99


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