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

Glutamate-mediated excitotoxicity is associated with adenosine triphosphate (ATP) degradation and generation of oxygen radicals. Hypoxanthine and lactate depict energetic impairment, while xanthine and uric acid reflect activity of radical producing xanthine oxidase. Cerebrospinal fluid (CSF) glutamate, hypoxanthine, lactate, xanthine, and uric acid were investigated in neurological patients. In multiple sclerosis, myelopathy, stroke, epilepsy and viral meningitis glutamate, hypoxanthine, xanthine, and uric acid are increased 2-3-fold compared to controls. Lactate is only elevated in meningitis. Normal lactate dehydrogenase (LDH) levels and absent correlation between the albumin ratio and neurochemical parameters exclude an artificial increase due to cell lysis and barrier damage. Absent correlation between neurochemical parameters within each patient group is most likely related to preserved glial and neuronal uptake mechanisms. CSF hypoxanthine, xanthine, and uric acid levels appear superior to lactate in reflecting glutamate-mediated excitotoxicity in neurological patients.
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PMID:Cerebrospinal fluid hypoxanthine, xanthine and uric acid levels may reflect glutamate-mediated excitotoxicity in different neurological diseases. 946 46

The Y chromosome in spontaneously hypertensive rats (SHR) and stroke-prone rats has been shown to contain a locus that contributes to the hypertensive effect; both the sympathetic nervous system and testosterone may be involved. The objective of this study was to look at the effects of testosterone on renal norepinephrine (NE) release and content in the isolated perfused kidney in different Y chromosome backgrounds. The study involved male SHR, Wistar-Kyoto rats (WKY), and 2 consomic strains with different Y chromosomes (n=5 to 8 per group). Adult animals were castrated, and implants containing testosterone propionate were placed at the base of the neck. Blood testosterone levels were measured by radioimmunoassay 2 weeks after castration. The left kidney was isolated and perfused with oxygenated Krebs solution at a constant flow and temperature with KCl and electrical stimulation of the renal nerves. Perfusate was collected and analyzed for NE by high-performance liquid chromatography. Lactate dehydrogenase analyses were performed as a marker for potential tissue damage. Renal perfusate and renal tissue NE levels were significantly elevated by testosterone. The average NE increase with a single testosterone implant was 13.2 ng/mL, and for a double testosterone implant it was 29.8 ng/mL. The Y chromosome from the SHR produced a significant increase in renal NE release compared with the WKY Y chromosome. Significance was shown between all groups: 1 versus 2 implants, P=0.0067; 1 versus sham implants, P=0.015; 2 versus sham implants, P<0.001. In conclusion, testosterone caused an enhanced renal NE release that was strain-specific, with the Y chromosome raising renal NE content and release.
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PMID:Testosterone effects on renal norepinephrine content and release in rats with different Y chromosomes. 982 48

Astrocytes cope more readily with hypoxic insults than do neurons. We hypothesized that astrocytes can upregulate their glycolytic capacity, allowing anaerobic glycolysis to provide sufficient ATP for cell survival as well as for carrying out critical functions such as taking up glutamate. To test this hypothesis, astrocytes were subjected to hypoxia for 5 hr. Lactate dehydrogenase (LDH) and pyruvate kinase activities increased 3- to 4-fold. Examination of LDH isoenzyme patterns determined that it was the anaerobic isoenzymes that were upregulated. To determine whether increase in enzyme activity translates into increased glycolytic capacity, astrocytes were subjected to varying time periods of hypoxia, and glucose uptake was measured under conditions where astrocytes were forced to consume more ATP. This demonstrated that 8 hr of hypoxia resulted in a doubling of glycolytic capacity. We suggest that how quickly astrocytes upregulate glycolytic capacity may determine whether or not neurons within the stroke penumbra survive.
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PMID:Astrocytes respond to hypoxia by increasing glycolytic capacity. 1039 3

During diving, marine mammals must rely on the efficient utilization of a limited oxygen reserve sequestered in the lungs, blood and muscles. To determine the effects of exercise and apnea on the use of these reserves, we examined the physiological responses of adult bottlenose dolphins (Tursiops truncatus) trained to breath-hold on the water surface or to dive to submerged targets at depths between 60 and 210 m. Changes in blood lactate levels, in partial pressures of oxygen and carbon dioxide and in heart rate were assessed while the dolphins performed sedentary breath-holds. The effects of exercise on breath-hold capacity were examined by measuring heart rate and post-dive respiration rate and blood lactate concentration for dolphins diving in Kaneohe Bay, Oahu, Hawaii. Ascent and descent rates, stroke frequency and swimming patterns were monitored during the dives. The results showed that lactate concentration was 1.1+/-0.1 mmol l(-1) at rest and increased non-linearly with the duration of the sedentary breath-hold or dive. Lactate concentration was consistently higher for the diving animals at all comparable periods of apnea. Breakpoints in plots of lactate concentration and blood gas levels against breath-hold duration (P(O2), P(CO2)) for sedentary breath-holding dolphins occurred between 200 and 240 s. In comparison, the calculated aerobic dive limit for adult dolphins was 268 s. Descent and ascent rates ranged from 1.5 to 2.5 m s(-1) during 210 m dives and were often outside the predicted range for swimming at low energetic cost. Rather than constant propulsion, diving dolphins used interrupted modes of swimming, with more than 75 % of the final ascent spent gliding. Physiological and behavioral measurements from this study indicate that superimposing swimming exercise on apnea was energetically costly for the diving dolphin but was circumvented in part by modifying the mode of swimming.
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PMID:The diving physiology of bottlenose dolphins (Tursiops truncatus). I. Balancing the demands of exercise for energy conservation at depth. 1050 10

Apoptotic cell death has been implicated in Alzheimer's disease pathology and amyloid peptide induced neurotoxicity. We investigated the survival promoting effects of Propentofylline in two models of apoptotic cell death, nerve growth factor withdrawal and beta-amyloid mediated cell death in nerve growth factor differentiated rat pheochromocytoma cell lines. The increase in cell death as measured by lactate dehydrogenase release in response to nerve growth factor withdrawal was suppressed by nitric oxide donor S-nitroso-N-acetylpenicillamine (12.5 to 200 microM) and by 8-bromoguanosine-3',5'-cyclic monophosphate (1.25 to 10mM). Both agents decreased cell death mediated by 25 microM beta-amyloid, suggesting that the protective mechanism involves guanosine -3', 5'-cyclic monophosphate. In support of this hypothesis we can show that S-nitroso-N-acetylpenicillamine increases intracellular levels of guanosine -3',5'-cyclic monophosphate in pheochromocytoma cell lines 3 to 8 fold.Propentofylline, a phosphodiesterase inhibitor, has previously demonstrated neuroprotective activity in stroke models and is a potential candidate for therapeutic treatment in neurodegenerative diseases. The present findings support this claim by providing evidence that Propentofylline has protective effects in both nerve growth factor withdrawal and beta-amyloid mediated cell death. Lactate dehydrogenase release was significantly reduced and caspase-3-like activity was attenuated after cotreatment with Propentofylline. Furthermore Propentofylline dose responsively increases intracellular guanosine-3',5'-cyclic monophosphate levels over the same dose range that provided protection. We hypothesized that guanosine-3',5'-cyclic monophosphate is a key mediator of neuroprotection under these conditions.
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PMID:Guanosine 3',5'-cyclic monophosphate mediated inhibition of cell death induced by nerve growth factor withdrawal and beta-amyloid: protective effects of propentofylline. 1097 37

The aim of the study was the assessment of concentrations of lactic acid in the blood of patients with mild course and severe course of ischaemic stroke in the earliest stage of the disease. The subject of the study were 20 patients with a mild ischaemic stroke and 20 patients with a severe one on its 1st, 3rd and 7th day. Enzymatic method for determining lactic acid content in the blood was used (the kits Test-Combination Lactate fully enzymatic of Boehringer Mannheim). In the group of patients with mild ischaemic stroke increase values of lactic acid were shown on all days of the disease, but the differences were statistically insignificant. In patients with severe ischaemic stroke these values were higher than in controls, and the differences were statistically significant. The study showed a positive correlation between high concentrations of lactic acid and severe clinical condition of patients.
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PMID:[Evaluation of lactic acid levels in blood of patients with ischemic stroke in the earliest stage of the disease]. 1110 72

Lactate production and expressions of monocarboxylate transporter 1 (MCT1) and lactate dehydrogenase (LDH) mRNA after hypoxia and reoxygenation (H/R) were examined by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) using astrocytes in culture isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY). The basal production of lactate in SHRSP was the same as that observed in WKY. In contrast the lactate levels in SHRSP at 1 and 6 h of reoxygenation after hypoxia were significantly lower than those observed in WKY. In addition LDH and MCT1 mRNA expressions in SHRSP were significantly less strong compared with those in WKY during H/R. These findings indicate that decreased production and slow transport of lactate in SHRSP astrocytes are involved in neuronal energy depletion and possibly encourage neuronal damage, although hereditary weakness of cortical neurons is also related to cell death during H/R.
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PMID:Reduced production of lactate during hypoxia and reoxygenation in astrocytes isolated from stroke-prone spontaneously hypertensive rats. 1110 94

The aim of this study is to investigate blood lactic acid levels after the placement of the AbioCor implantable replacement heart to determine whether circulatory support with the AbioCor device results in adequate tissue perfusion. Tissue perfusion may not be adequate during cardiac surgery, especially with the use of cardiopulmonary bypass (CPB). Inadequate perfusion is usually associated with anaerobic metabolism, metabolic acidosis, and lactate accumulation. Ten calves had implantation of the AbioCor by means of a right thoracotomy. Standard cardiopulmonary bypass was performed during surgery. Lactic acid levels and blood gas analyses were measured. All animals were monitored for pressures in the aorta, pulmonary artery, and left and right atria. The output of the AbioCor was calculated based on beat rate and stroke volume. All animals were rapidly weaned off cardiopulmonary bypass to full AbioCor support and had normal hemodynamics with normal filling pressures. The lactic acid levels were elevated after surgery, peaked at 8 to 12 hours, and then gradually decreased to the normal range 24 hours after surgery. There was a positive relationship between lactate levels, oxygen consumption, and extraction rate, that is, the lactic acid levels were higher in the presence of increased oxygen consumption and increased oxygen extraction rate. There was a negative relationship between lactate levels and oxygen delivery, and arterial and venous oxygen content, that is, the lactic acid levels were higher when oxygen delivery and arterial and venous oxygen contents were low. The pathophysiology of lactic acidosis is uncertain, but is most likely due to inadequate perfusion during cardiopulmonary bypass, and lactate washout after adequate perfusion has been established. The return to aerobic metabolism with clearance of lactate demonstrates that the AbioCor is able to provide complete circulatory support with normal tissue perfusion.
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PMID:Blood lactic acid levels after artificial heart implantation. 1173 Feb 11

Cerebral tissue with T2 magnetic resonance imaging (MRI) abnormalities following stroke is generally considered infarcted, while surrounding regions with normal MRI appearance are believed to be healthy. To assess whether these surrounding regions consist of normal tissue, we explored the distribution of N-acetylaspartate (NAA) and lactate within and around the hyperintense area on T2-weighted MRI using proton MR spectroscopy. The study was carried out in 25 patients with middle cerebral artery occlusion imaged between 1 and 42 days after stroke onset. NAA/choline (Cho) ratios were significantly reduced in both areas of T2 hyperintensity and in surrounding tissue. The reduction was greater in the region of T2 hyperintensity than in the surrounding region (-50% vs. -28%, respectively) and was unrelated to the delay after the ictus. Lactate/Cho ratios increased massively within the abnormal T2 area, but did not differ from control values beyond the margin of hyperintensity. Overall data indicate that T2 visible lesions on MRI do not infer the entire injured tissue.
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PMID:Spectroscopic data following stroke reveal tissue abnormality beyond the region of T2-weighted hyperintensity. 1208 46

We describe the metabolic changes in the blood that appeared during a maximal 400-m swimming test in 7 male swimmers by Fourier-transform infrared spectrometry (FT-IR spectrometry). A 400-m test (255.9 +/- 6.8 s) was performed during which stroke frequency and time to complete each pool distance were recorded. In three other tests, the first 100 m, 200 m, and 300 m were swam at the same stroke frequency and velocity. Capillary blood samples were taken at rest and after tests to analyze change in plasma contents by FT-IR spectrometry. Best swimmers were characterized by higher glycemia increase at the onset of exercise (r = -0.91; p < 0.01). Lactate increase was also higher after 300 m (r = -0.97; p < 0.01). Higher amounts of fatty acids were also available at the end of exercise, as assessed by the relationships found between swimming velocity and concentrations of albumin (r = 0.96; p < 0.01), apolipoprotein C 3 (r = 0.93; p < 0.01), triglycerides (r = -0.81; p < 0.05), and fatty acids (r = 0.97; p < 0.01). This metabolic response allowed the best swimmers to maintain longer their initial swimming velocity. The best swimmers presented also higher amino-acid concentration increase during exercise (r = 0.91; p < 0.01). Therefore, performance competence originated probably from better regulation in carbohydrate, lipid, and amino-acid metabolism.
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PMID:Fourier-transform infrared spectrometry determination of the metabolic changes during a maximal 400-meter swimming test. 1286 40


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