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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We measured cerebral metabolic rates for glucose (CMRGlc) in the remote brain areas of 7 patients, who were affected by unilateral cortical infarction, at a chronic stage using 2[18F]-fluoro-2-deoxy-D-glucose and positron emission tomography. There were significant decreases of CMRGlc compared with each control value (p < 0.01), not only in the cerebral cortex directly damaged by the ischaemic insult, but also in the ipsilateral thalamus and in the contralateral cerebellum, areas in which no lesions had been detected by MRI or CT scan. The present study indicates that different mechanisms may be responsible for multi-focal metabolic disturbances in the remote areas after stroke. We suggest that these multi-focal brain dysfunctions may exacerbate clinical symptoms at a chronic stage of stroke.
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PMID:Multi-focal metabolic disturbances in human brain after cerebral infarction studied with 18FDG and positron emission tomography. 806 4

We have reported that exo-focal delayed neuronal damage was observed in the ipsilateral thalamus and the substantia nigra of the rat brain after occlusion of the middle cerebral artery (MCA). To determine if that phenomenon also occurs in humans, we measured cerebral metabolic rates for glucose (CMRGlc) in the remote brain areas at a chronic stage after cortical infarction using 2-[18F]fluoro-2-deoxy-D-glucose and position emission tomography (PET). The subjects studied were 11 patients who were affected by unilateral cerebral infarction in the cortex supplied by MCA. There were significant decreases of CMRGlc as compared with control values (p < 0.01), not only in the cerebral cortex directly damaged by the ischemic insult, but also in the ipsilateral thalamus and in the contralateral cerebellum, areas in which no lesions had been detected by MRI or CT scan. The present study indicates that different mechanisms may be responsible for multi-focal metabolic disturbances in the remote areas after stroke. The reduction of CMRGlc in the contralateral cerebellum may be explained by the crossed cerebellar diaschisis theory and in the ipsilateral thalamus as being due to retrograde degeneration associated with the infarcted cortex. We suggest that these multi-focal brain dysfunctions caused by neuronal network disturbances may exacerbate clinical symptoms at a chronic stage of stroke.
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PMID:Metabolic disturbances in exo-focal brain areas after cortical stroke studied by positron emission tomography. 806 8

The aim of this study was to compare the effectiveness of subcutaneous and intravenous fluid therapy in hydrating, elderly acute stroke patients. Thirty-four such patients, needing parenteral fluids because of impaired consciousness or dysphagia, were randomly allocated to receive either subcutaneous or intravenous fluids (2 litres of dextrose-saline/24 hours). Serum osmolality was measured before starting fluid therapy (Day 1) and on Days 2 and 3. An analysis of covariance of the osmolalities showed no statistical difference between the two groups (P = 0.12). The total cost of cannulae used over the 3 days for the subcutaneous route was approximately a third of that for the intravenous route. Complication rates were similar for the two groups. The results suggest that subcutaneous fluid therapy is an effective alternative to the intravenous route.
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PMID:A comparison of intravenous and subcutaneous hydration in elderly acute stroke patients. 818 52

Stroke prone spontaneously hypertensive rats (SHRSP) were less susceptible to stress in gastric lesions than Wistar-Kyoto rats used as normotensive controls. The gastric lesions induced by water-immersion restraint (WIR) in SHRSP were aggravated by pretreatment with 6-hydroxydopamine (6-OHDA), an agent for chemical sympathectomy, following decreases in blood pressure and sympathetic nerve function. 6-OHDA treatment remarkably reduced norepinephrine content but caused increases in dopamine content and in choline acetyltransferase activity in the stomach. The mechanism of aggravation of gastric lesions in SHRSP was investigated with regard to gastric acid and motility. The pretreatment with 6-OHDA of SHRSP significantly increased the acid secretion stimulated by 2-deoxy-D-glucose indirectly acting on parietal cells via the vagus nerve, but did not change the acid secretions stimulated by carbachol, pentagastrin and histamine acting directly on parietal cells. Gastric (corpus) motility associated with WIR was completely blocked by atropine. The pretreatment with 6-OHDA in SHRSP decreased the gastric motility during WIR, which was facilitated by treatment with domperidone. These results indicate that the sympathetic hyperactivity of the stomach prevents WIR-induced gastric lesion formation mainly via the inhibition of gastric acid secretion.
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PMID:The role of sympathetic neurons for low susceptibility to stress in gastric lesions. 832 Oct 86

1. Haemodynamic and hormonal responses to infused angiotensin II were studied in conscious salt-deplete dogs during infusion of D-glucose or losartan (DuP753/MK954). 2. Mean arterial pressure (118 +/- 13 mmHg) fell rapidly after losartan (60 min 106 +/- 18 mmHg) with a rise in heart rate (107 +/- 16 beats/min) from baseline (98 +/- 17 beats/min). Pressor responses to angiotensin II during D-glucose infusion (6 ng min-1 kg-1, 99 +/- 10 mmHg; 18 ng min-1 kg-1, 140 +/- 15 mmHg; 54 ng min-1 kg-1, 157 +/- 12 mmHg; 162 ng min-1 kg-1, 178 +/- 14 mmHg) showed a parallel shift during losartan infusion with very similar pressures in response to higher rates of angiotensin II infusion (54 ng min-1 kg-1, 108 +/- 17 mmHg; 162 ng min-1 kg-1, 138 +/- 14 mmHg; 486 ng min-1 kg-1, 155 +/- 14 mmHg; 1458 ng min-1 kg-1, 177 +/- 12 mmHg). Losartan caused a fall in baseline systemic vascular resistance. Despite the similar mean arterial pressure, the rise in systemic vascular resistance after angiotensin II during D-glucose infusion (162 ng min-1 kg-1, 8065 +/- 1967 dyn s cm-5) was reduced during losartan infusion (1458 ng min-1 kg-1, 6645 +/- 1720 dyn s cm-5. Losartan caused a small rise in cardiac output related to a rise in heart rate and increased stroke volume. Pressure infusions of angiotensin II caused a fall in cardiac output during D-glucose infusion, which was blocked during losartan infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemodynamic and hormonal responses to losartan (DuP753/MK954) infusion during cardiac catheterization in conscious salt-deplete dogs. 840 84

The prototypical integrin receptor, alpha IIb beta 3, isolated from the membrane fraction of human blood platelets by solubilization in Triton X-100 (reduced) and affinity chromatography on lentil lectin-agarose, has been further purified by gel filtration chromatography in octyl glucoside to obtain the intact receptor complex in a form suitable for hydrodynamic measurements. The molecular weight [(6.0 +/- 0.2) x 10(3)] and Stokes radius (2.3 +/- 0.1 nm) of detergent micelles formed in 0.03 M octyl glucoside have been determined by classical light scattering intensity and dynamic light scattering measurements, respectively. An algorithm has been developed which explicitly considers the contribution of detergent micelles to the intensity autocorrelation function of particles suspended in detergent. This procedure has been validated with polystyrene particles of known radius, as well as with the soluble protein fibrinogen. Application of these procedures to dynamic light scattering data obtained with alpha IIb beta 3 resulted in a translational diffusion coefficient (Dto(20,w)) of (2.78 +/- 0.31) x 10(-7) cm2 s-1, corresponding to a Strokes radius (Rs) of 7.67 +/- 0.85 nm for the integrin/octyl glucoside complex. Light scattering intensity measurements gave a molecular weight of (2.26 +/- 0.22) x 10(5) for the polypeptide moiety of the complex, in excellent agreement with the 2.28 x 10(5) value calculated from primary structure data. As a spherical, hydrated alpha IIb beta 3 complex, with bound detergent, would exhibit a Stokes radius of approximately 5 nm, these data indicate considerable asymmetry in the solution conformation of alpha IIb beta 3.
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PMID:Dynamic light scattering studies of alpha IIb beta 3 solution conformation. 847 5

In a randomized double-blind placebo-controlled study in 30 patients with acute ischemic stroke, the effect of the adenosine uptake blocker propentofylline on regional brain glucose metabolism (rCMRglu) was investigated using repeated positron emission tomography (PET) with 2-[18F]fluoro-2-deoxy-D-glucose (FDG). Treatment was initiated within 48 h after onset of symptoms. The clinical course was followed for 3 months. In the propentofylline group, after 14 days rCMRglu was increased in the infarct by 37.3% and was practically unchanged in other brain regions, whereas in the control group glucose metabolism had decreased in all regions (1.4-13.4%). These differences were significant between the two groups [Analysis of variance (ANOVA) p = 0.005]. Although there was a trend toward greater clinical improvement in the propentofylline-treated patients, this did not reach statistical significance. The results correspond to experimental data showing that propentofylline improves energy metabolism in cerebral ischemia. A clinical trial is needed to determine whether this new therapeutic principle can be successfully used in acute human stroke.
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PMID:Effect of propentofylline on regional cerebral glucose metabolism in acute ischemic stroke. 847 10

We reported previously that genetic polymorphisms of the alpha 2-adrenergic receptor are associated with hyperinsulinemia, diabetes mellitus, and hypertension in blacks. The evolutionary driving force for maintaining such deleterious mutations in the black population is unknown. Recognizing that vascular alpha 2-adrenergic receptors mediate cold-induced vasoconstriction and that temperature maintenance is a primary thrust of cellular metabolism, we postulated that vascular alpha 2-adrenergic receptors contribute significantly to metabolic heat generation in homeotherms such as humans. Using aerobic lactate production as an indicator of thermogenesis, we measured metabolic heat production in HT29 cells that expressed the gene encoding human vascular alpha 2-adrenergic receptors. Epinephrine, an alpha 2-adrenergic receptor agonist, increased net lactate efflux from 226 +/- 20 to 280 +/- 20 nmol/min (mean +/- SE) (P = .06). Clonidine, a more specific alpha 2-adrenergic agonist, increased lactate efflux from 110 +/- 6 to 156 +/- 8 nmol/min (P < .01). Similarly, in the presence of physiological concentrations of glucose (5.5 mmol/L), insulin increased lactate production from 123 +/- 6 to 175 +/- 10 nmol/min (P < .01). Because differences in aerobic glycolysis may also explain the heat intolerance and abnormal fuel homeostasis found in genetically hypertensive rats, we also measured lactate production in cultured vascular smooth muscle cells isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive control Wistar-Kyoto rats (WKY). Vascular smooth muscle cells from SHRSP had significantly greater lactate efflux compared with cells from normotensive WKY (296 +/- 4 versus 172 +/- 2 nmol/min, P < .001). These differences were not due to abnormalities in glucose uptake, as lactate efflux was greater in SHRSP cells compared with WKY cells when dextrose was replaced with equimolar concentrations of fructose (230 +/- 6 versus 138 +/- 2 nmol/min, P < .001). alpha 2-Adrenergic agonists increase lactate efflux in HT29 cells, and abnormalities in vascular smooth muscle lactate metabolism in genetically hypertensive rats is independent of altered glucose uptake. These data provide support for our hypothesis that balanced polymorphisms of the alpha 2-adrenergic receptor could offer protection against cold stress by increasing the thermogenic response associated with aerobic lactate production.
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PMID:Alpha 2-adrenergic agonists increase cellular lactate efflux. 862 Dec 3

To search for possible effect of dehydroepiandrosterone sulfate (DHAS) on maternal cardiac function in term pregnancy, impedance cardiographic assessments were made on 15 normal full-term pregnant women before and 5, 10, 15, 20, 25, and 30 minutes after the administration of a 200 mg intravenous dose of DHAS in 20 mL of 5% dextrose. The cardiac output, stroke volume, heart rate, and mean arterial pressure were recorded. Maternal cardiac output increased from baseline by 20% (p < 0.05) after 15 minutes and the mean increase in stroke volume was 25% (p < 0.05) after 15 minutes. No change was found in heart rate or mean arterial blood pressure. DHAS induces a significant increase in both maternal stroke volume and cardiac output without change in heart rate or mean arterial pressure, which suggests a possible increase in cardiac contractility in term pregnancy.
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PMID:Effect of dehydroepiandrosterone sulfate on maternal cardiac function in term pregnancy. 864 78

The effects of TDN-345 on mortality and ischemic neurological deficit following transient global cerebral ischemia in Mongolian gerbils and also the rate of local cerebral glucose utilization (LCGU) in stroke-prone spontaneously hypertensive rats (SHRSP) with cerebrovascular lesions were investigated. In Mongolian gerbils, ischemia was produced by clamping the bilateral common carotid arteries for 15 min. TDN-345 (0.1-1.0 mg/kg) dose-dependently decreased the mortality and ischemic neurological deficit score when administered orally twice, 60 min before ischemia and 90 min after recirculation. Additionally, TDN-345 (0.2 or 1.0 mg/kg, p.o. once daily for 3 weeks after the onset of stroke) decreased the mortality and recurrence of stroke in SHRSP. To determine the site of action of TDN-345 in the brain, the rate of LCGU in various brain regions in SHRSP with stroke was examined using a [14C]2-deoxy-D-glucose method. The rate of LCGU decreased significantly in all the brain regions in SHRSP with stroke compared with Wistar-Kyoto (WKY) control rats, whereas the reduction in the rate of LCGU in SHRSP with stroke was prevented by TDN-345 treatment, especially in the sensorimotor cortex and locus coeruleus. These results suggest that TDN-345 has therapeutic efficacy in the treatment of cerebrovascular disease.
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PMID:Beneficial effects of TDN-345, a novel Ca2+ antagonist, on ischemic brain injury and cerebral glucose metabolism in experimental animal models with cerebrovascular lesions. 926 74


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