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)

Carotid duplex ultrasonography is the noninvasive procedure of choice for evaluating ECAD. However, carotid angiography should be performed before doing carotid endarterectomy. Multivariate logistic regression analysis showed that significant prognostic variables for ECAD in an elderly population are (1) cigarette smoking, (2) serum total cholesterol, (3) serum HDL cholesterol (inverse association), (4) diabetes mellitus, and (5) prior CAD. Patients with 80-100% ECAD develop a higher incidence of ABI and TIA than patients with 40-80% ECAD. Patients with 40-80% ECAD develop a higher incidence of ABI and TIA than patients with 0-40% ECAD. Patients with ECAD have a higher prevalence of prior CAD and develop a higher incidence of new coronary events than patients without ECAD. In patients with ECAD, significant prognostic variables for new coronary events are (1) silent ischemia, (2) prior CAD, (3) serum HDL cholesterol (inverse association), and (4) cigarette smoking. Risk factors for ECAD and CAD should be treated in patients with ECAD. Cigarette smoking must be stopped. Hypertension, dyslipidemia, and diabetes mellitus should be treated. Aspirin, 325 mg/d, should be administered to patients with ECAD. Ticlopidine hydrochloride, 250 mg two times per day should be considered in patients with ECAD who are unable to tolerate aspirin or who develop cerebrovascular events on aspirin. Carotid endarterectomy should be considered in symptomatic patients with 70-99% ECAD.
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PMID:Extracranial carotid arterial disease. 818 62

Transient cerebral ischemia causes long-lasting inhibition of protein synthesis despite recovery of energy metabolism. We investigated the question if this inhibition is due to the formation of a suppression factor which interferes with the function of the protein synthesizing machinery. For this purpose rats were submitted to 20 minutes four vessel-occlusion followed by recirculation times from 30 minutes to 7 days. Post-mitochondrial supernatant (PMS) from various brain regions was added to a self-contained, cell-free rabbit reticulocyte translational system, and the effect on in vitro protein synthesis was assessed by measuring 14C-leucine incorporation over a duration of 45 minutes. PMS prepared at the end of ischemia from hippocampus, striatum and cerebellum inhibited in vitro protein synthesis by 40%-60% but there was only a minor inhibition by PMS from cerebral cortex. During post-ischemic recirculation cortical PMS transiently induced inhibition of in vitro protein synthesis by 30% but this effect gradually disappeared within one week. The inhibition caused by PMS from hippocampus, striatum and cerebellum was not reversed during recirculation and still amounted to about 40% after 7 days. Inhibition of in vitro protein synthesis could be blocked by heating PMS to 100 degrees C, indicating that the suppressor factor is a protein. The comparison of the in vitro effect of postischemic PMS with previously described in vivo inhibition of protein synthesis demonstrates that the here observed suppressor factor is not able to explain the overall disturbance of protein synthesis in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of global ischemia and recirculation of rat brain on protein synthesis in vitro. 819 40

We report on eight children who suffered from cerebrovascular ischemia or stroke at the age of 2 or up to 11 years. Antiphospholipid antibodies (APLA) were detected in two cases during the ischemic event and in six cases during follow-up examinations (after six weeks or within a span of six years). In two patients multiple stenoses of basal cerebral arteries were found; one of them suffered from moyamoya syndrome. The acute hemiplegia in one patient was linked to an asymptomatic mycoplasmal infection and APLA. In three cases, one of the parents was also APLA-positive. Seven patients were treated with acetylsalicylic acid, and in four cases immunoglobulin infusions were given. Transient ischemic attacks subsided after the child with the moyamoya syndrome received immunoglobulins. No effect of medication could be established in the other children. The concept of the antiphospholipid syndrome is still evolving. As none of the common risk factors pertaining to strokes in adults apply to children, pediatric research may offer a suitable platform for specific investigations on the causal, pathogenetic role of APLA. We propose that all children suffering from stroke or transient ischemic attacks should be tested for APLA.
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PMID:Antiphospholipid antibodies in cerebrovascular ischemia and stroke in childhood. 820 57

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

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

Transient cerebral ischemia can produce irreversible neuronal damage and permanent learning and memory impairments in humans. This study examined whether ischemia-induced brain damage in rats results in impairments on the delayed nonmatching-to-sample (DNMS) task, a nonspatial recognition task analogous to tests on which amnesic patients display impairments. Male Wistar rats received either sham surgery or 20-min forebrain ischemia induced by bilateral carotid occlusion and hypotension. Four weeks after surgery, ischemic rats were significantly impaired in both learning and performing the DNMS task at retention intervals up to 5 min. Extensive presurgical training did not reduce this impairment. Observable cell loss in ischemic rats was limited to CA1 pyramidal neurons and a subset of cells in the dentate gyrus. The results indicate that ischemic damage to the hippocampus in rats results in recognition memory deficits similar to those produced by ischemic damage in humans.
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PMID:Impaired object recognition memory in rats following ischemia-induced damage to the hippocampus. 844 57

Transient ischemic attacks (TIAs) are not homogeneous and may consist of subsets with mechanisms as varied as their stroke counterparts. We describe a form of TIA in 50 patients where crescendo episodes of ischemia were restricted to the region of the internal capsule, usually causing symptoms affecting face, arm, and leg. These patients composed 4.5% of a consecutive series of patients admitted with TIAs over a 15-year period and 33% of all TIAs classified as subcortical. We believe that the ischemia was most often due to hemodynamic phenomena in diseases, single, small penetrating vessels. When cerebral infarction developed, it was usually lacunar and involved a single penetrating vessel, although occasionally striatocapsular or anterior choroidal artery territory infarction occurred. There was no evidence of artery-to-artery or heart-to-artery embolism. Resistance to various forms of therapy, including hemodiluting, anticoagulant, and thrombolytic agents, was common. Because of dramatic and easily recognizable clinical presentation, apparent specific pathophysiologic mechanism, and the development of early capsular stroke in a high proportion of cases (42%), we have termed this the "capsular warning syndrome."
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PMID:The capsular warning syndrome: pathogenesis and clinical features. 829 82

After a transient ischemic attack of the cardiac vascular system, reactive oxygen-derived free radicals, including the superoxide (O2-.) and hydroxyl (.OH) radicals can be easily produced during reperfusion. These free radicals have been suggested to be responsible for reperfusion-induced cardiac stunning and reperfusion-induced arrhythmia. Hydrogen peroxide (H2O2) is often used as an experimental source of oxygen-derived free radicals. Using freshly dissociated single rat cardiac myocytes and the rat cardiac myoblast cell line, H9c2, we have shown, for the first time, that an intriguing pHiota acidification (approximately 0.24 pH unit) is induced by the addition of 100 micromol/L H2O2 and that this dose is without effect on the intracellular free Ca2+ levels or viability of the cells. Using H9c2 as a model cardiac cell, we have shown that it is the intracellular production of .OH, and not O2-. or H2O2, that results in this acidification. We have excluded any involvement of (1) the three known cardiac pHi regulators (the Na+-H+ exchanger, the Cl--HCO3 exchanger, and the Na+-HCO3 co-transporter), (2) a rise in intracellular Ca2+ levels, and (3) inhibition of oxidative phosphorylation. However, we have found that H2O2-induced acidosis is due to inhibition of the glycolytic pathway, with hydrolysis of intracellular ATP and the resultant intracellular acidification. In cardiac muscle and in skinned cardiac muscle fiber, it has been shown that a small intracellular acidification may severely inhibit contractility. Therefore, the sustained pHi decrease caused by hydroxyl radicals may contribute, in some part, to the well-documented impairment of cardiac mechanical function (ie, reperfusion cardiac stunning) seen during reperfusion ischemia.
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PMID:Mechanism of hydrogen peroxide and hydroxyl free radical-induced intracellular acidification in cultured rat cardiac myoblasts. 863 13

We conducted a retrospective analysis examining the relationship between the tumor quality and the occurrence of systemic embolization in 16 patients who underwent surgical excision of the left atrial myxoma. Systemic embolization occured in 10 patients (63%) before surgery, in 5 of whom embolic episodes were the first manifestation of the tumor. Cerebral infarction had developed in 7 patients, TIA in 2, myocardial infarction in 2, limb ischemia in 2, and multiple infarctions in the kidney, adrenal gland, spleen and bone marrow in one. A permanent deficit remained in 6 patients (60%). Myxoma was a lobulated and gelatinous type in 9 (90%) of these patients with embolization and a solid type only in one case. When the dignosis of the left atrial myxoma with soft and fragile quality is made by echocardiography, surgical excision should be performed without delay to prevent systemic embolization.
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PMID:[Clinical analysis of embolism with left atrial myxomas]. 872 62

In 154 subjects (age 63 +/- 11 years; 63 women and 91 men) randomly selected from the population, we tested the hypothesis that inflammatory parameters are associated with vascular risk factors and particularly with a history of ischemic vascular diseases. The subjects were part of the control group (n = 197) in a case-control study investigating recent infection as a risk factor for acute cerebrovascular ischemia and had been matched for sex and age with patients suffering from acute ischemic stroke or transient ischemic attack. Subjects with malignant or inflammatory diseases, with recent trauma, surgery or vascular diseases (n = 43) were excluded from the present analysis. In multivariate analysis, current smoking, diabetes mellitus, age > or = 65 years, and a history of stroke independently increased the leukocyte count. Hypertriglyceridemia, peripheral arterial disease, and diabetes mellitus were positively associated with C -reactive protein (CRP). Age > or = 65 years and diabetes mellitus independently increased fibrinogen. (p < 0.05, respectively) Subjects with a history of cerebrovascular, cardiovascular or peripheral arterial disease had higher leukocyte counts, fibrinogen and CRP than subjects without vascular risk factors and higher leukocytes and fibrinogen than subjects with one or more risk factors. Subjects under the age of 65 with vascular risk factors but without ischemic diseases had higher leukocyte count, fibrinogen and CRP and subjects older than 65 with risk factors had higher CRP than subjects without risk factors or ischemic diseases in the same age group. (p < 0.05, respectively) These results support the hypotheses that low-grade inflammation is associated with vascular risk factors and that inflammatory mechanisms may contribute to the risk of organ ischemia.
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PMID:The association of leukocyte count, fibrinogen and C-reactive protein with vascular risk factors and ischemic vascular diseases. 873 28


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