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

A universal peroxyoxalate-chemiluminescence detection system for high performance liquid chromatography, available for a variety of mobile phases, has been developed. The system consisted of a dual-head short-stroke pump and a chemiluminescence detector. The standard conditions using bis(2,4,6-trichlorophenyl) oxalate (TCPO) as aryl oxalate were as follows. The first postcolumn solution was the mixture of 0.5 M imidazole-nitric acid (pH 7.5) and acetonitrile (1:4, v/v). The second was acetonitrile containing TCPO-hydrogen peroxide. These two solutions were delivered by the two pump-heads. After the pH of the column eluate was adjusted to the optimum range (6.5-7.5) by the first postcolumn solution, the solution was mixed with the second postcolumn solution. After flowing through a reaction coil, the chemiluminescence of the mixture was monitored. Using this system, a high sensitivity (fmol level) was obtained for perylene as an analyte with mobile phases having different pH values (2.0-8.0). Polycyclic aromatic hydrocarbons became detectable to a high sensitivity even after the column separation using an acidic mobile phase. The detection sensitivity of nitrated pyrenes after on-line electrochemical reduction using an acidic mobile phase was also increased. This system might be available for other aryl oxalates by some modifications of the postcolumn solutions.
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PMID:A universal peroxyoxalate-chemiluminescence detection system for mobile phases of differing pH. 163 95

The appearance of acute cerebral infarction was evaluated on MR images and CT scans obtained in 31 patients within 24 hr of the ictus; follow-up examinations were performed 7-10 days later in 20 of these patients and were correlated with the initial studies. Acute infarcts were visible more frequently on MR images than on CT scans (82% vs 58%). Proton density- and T2-weighted scans usually demonstrated regions of hyperintensity corresponding to acute infarcts, but proton density-weighted scans often showed better definition of the lesion in terms of regional anatomy. Follow-up MR images and CT scans identified approximately 88% of subacute strokes, 54% of which were better defined and/or larger than on the initial examination. In 20% of lesions, "hemorrhagic" characteristics were seen on at least one examination. CT and MR imaging were comparable in delineating acute hemorrhage, but MR detected more cases with evidence of hemorrhage on follow-up examinations. MR appears to be more sensitive than CT in the imaging of acute stroke.
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PMID:Diagnosis of acute cerebral infarction: comparison of CT and MR imaging. 156 33

Proton nuclear magnetic resonance spectroscopy is a unique method to monitor noninvasively the concentrations of cerebral metabolites. N-Acetyl-L-aspartate, the concentration of which is assumed to be stable during hypoxia, has been used to form ratios with lactate. To determine the stability of the signal from N-acetyl-L-aspartate, we used a model of graded hypoxia in rats to monitor the percentage changes from baseline of the peak heights for lactate, lipids, and N-acetyl-L-aspartate. Anesthetized adult rats were exposed sequentially to 15% and 10% O2 while proton nuclear magnetic resonance spectra were collected with a surface coil in a 7-T 89-mm-bore spectrometer. Brain lactate concentration was either increased by feeding or infusion of glucose (n = 9) or lowered by fasting (n = 7). After death the brains were removed and frozen, and the water- and lipid-soluble compounds were extracted to identify the origin of the signals. We analyzed the data both as the percentage change from baseline for heights of the lactate (1.33 ppm), lipids (1.5 ppm), and N-acetyl-L-aspartate (2.02 ppm) peaks and as the ratios of heights of the 1.33 and 2.02 and the 1.5 and 2.02 ppm peaks. Both hypoxic episodes caused a 45% decrease from baseline in the 2.02 ppm peak. During the second hypoxic episode, the 1.33:2.02 ppm peak height ratio increased significantly in hyperglycemic rats (p less than 0.05) but was unchanged in hypoglycemic rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Jan
PMID:Effect of hypoxia on cerebral metabolites measured by proton nuclear magnetic resonance spectroscopy in rats. 184 48

A dual-head short-stroke pump has two advantages in the post-column peroxyoxalate chemiluminescence (PO-CL) detection system. The first is to increase the mixing efficiency of solutions. The second is to increase the stability of the PO-CL reaction by keeping the aryl oxalate and hydrogen peroxide solutions separate. The detection sensitivities for six polycyclic aromatic hydrocarbons (PAHs) increased in the present system by using bis(2,4-dinitrophenyl) oxalate (DNPO) or bis(2,3,4,5,6-pentafluorophenyl) oxalate (PFPO) instead of such popular aryl oxalates as bis(2,4,6-trichlorophenyl) oxalate (TCPO) and bis[2-(3,6,9-trioxadecyloxycarbonyl)-4-nitrophenyl] oxalate (TDPO). Both DNPO and PFPO increased the sensitivities by factors of 4.1-10.2 and 3.5-8.1, respectively. In addition, DNPO was more stable than PFPO in acetonitrile. These results suggest that DNPO is the most useful aryl oxalate for the sensitive PO-CL detection of PAHs.
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PMID:Effect of a dual-head short-stroke pump on post-column peroxyoxalate chemiluminescence detection. 191 22

Bradykinin produces less dilatation of pial arterioles in stroke-prone spontaneously hypertensive rats than in normotensive Wistar-Kyoto rats. The goals of this study were to determine the mediator of bradykinin-induced dilatation in cerebral arterioles of rats and to determine whether responses to this mediator are altered in hypertensive rats. Diameter of pial arterioles (20-65 microns) was measured using intravital microscopy in 18 normotensive and 17 hypertensive rats. Superfusion of 3 x 10(-7) M bradykinin dilated pial arterioles by 53 +/- 4% (mean +/- SEM) in normotensive rats but only 33 +/- 6% in hypertensive rats (p less than 0.05 versus normotensive rats). Vasodilatation in response to bradykinin was almost completely inhibited by 280 units/ml catalase in both normotensive and hypertensive rats (n = 7 and n = 7, respectively) whereas 150 units/ml superoxide dismutase (n = 6 and n = 5, respectively) and 1 mM deferoxamine (n = 5 and n = 5, respectively) did not attenuate bradykinin-induced vasodilatation. These findings suggest that hydrogen peroxide is the mediator of bradykinin-induced dilatation in cerebral arterioles of rats. We also examined responses of cerebral arterioles to hydrogen peroxide in five normotensive and six hypertensive rats. Dilator responses of cerebral arterioles to 3.2 x 10(-5) M to 1.6 x 10(-4) M hydrogen peroxide did not differ in normotensive and hypertensive rats, which suggests that impaired dilatation of cerebral arterioles in response to bradykinin is not related to altered responsiveness of smooth muscle to an endothelium-derived relaxing factor.(ABSTRACT TRUNCATED AT 250 WORDS)
Stroke 1991 Sep
PMID:Mechanisms of impaired endothelium-dependent cerebral vasodilatation in response to bradykinin in hypertensive rats. 192 61

Proton magnetic resonance (MR) imaging has been recommended as a diagnostic tool for the detection of focal cerebral ischemia. We compared microscopic MR images of rat brains after focal cerebral ischemia with evidence of histological damage found on corresponding silver-impregnated or cresyl violet-stained brain sections. Ten male Wistar rats were subjected to permanent unilateral occlusions of the right middle cerebral and common carotid arteries under halothane anesthesia. Twenty-four hours later the area of injury on MR images amounted to 26% of the total slice area, whereas only 9% of the total slice area was necrotic on histological sections from the same animals. The infarcted areas on tissue sections were surrounded by regions of selective neuronal injury in the cerebral cortex and occasionally in the hippocampus. The area of injury on MR images was larger than the combined areas of infarction and selective neuronal injury on histological sections. Areas of increased T2 values on MR images extended medially into noninfarcted striatum and laterally and dorsally into noninfarcted cortex. The lateral and dorsal areas on MR images frequently coincided with cortical areas in which considerable selective neuronal injury was present in the upper cortical layers. We hypothesize that the abnormal areas on MR images above histologically normal brain tissue represent the ischemic penumbra. If true, this is the first demonstration of the ischemic penumbra by MR imaging and may reflect our use of Wistar rats, a new image analysis technique, and ultra-high resolution MR imaging.
Stroke 1991 Feb
PMID:Quantitative proton magnetic resonance imaging in focal cerebral ischemia in rat brain. 200 91

Infusion of 400 microliters air into the left internal carotid artery of five anesthetized rabbits caused transient pial arteriole air embolism, an immediate 41.9 +/- 0.8% dilatation of the embolized vessels, suppression of the cortical somatosensory evoked response to 29.4 +/- 2.7% of baseline, and a progressive decline in ipsilateral cerebral blood flow (measured by hydrogen clearance) to 46 +/- 4.1% of baseline after 2 hours. These values were significantly different from those at baseline and from the responses of 10 control rabbits given equivalent intracarotid saline infusions. Twelve other rabbits were made leukopenic by treatment with 1.5 mg/kg i.v. mechlorethamine 72 hours prior to study. Mean +/- SEM leukocyte count decreased from 6,320 +/- 73/mm3 to 1,890 +/- 66/mm3 without any change in the leukocyte differential or erythrocyte and platelet counts. Intracarotid infusion of saline into seven of the leukopenic rabbits caused no changes. In the other five leukopenic rabbits, infusion of 400 microliters air caused air embolism but did not produce the anticipated declines in cerebral blood flow or the cortical somatosensory evoked response, both of which remained indistinguishable from baseline values and responses in the seven saline-treated leukopenic controls. Similarly, air-embolized arterioles showed nonsignificant dilatation in leukopenic rabbits. Our data suggest that the decreases in both cerebral blood flow and brain function seen after air embolism require the presence of leukocytes.
Stroke 1991 Mar
PMID:Air embolism of the brain in rabbits pretreated with mechlorethamine. 200 4

It is now becoming increasingly clear that free radicals contribute to brain damage in several conditions, such as hyperoxia and trauma. It has been more difficult to prove that free radical production mediates ischemic brain damage, but it has often been suggested that it may be a major contributor to reperfusion damage, observed following transient ischemia. Recent results demonstrate that cerebral ischemia of long duration, particularly when followed by reperfusion, leads to enhanced production of partially reduced oxygen species, notably hydrogen peroxide (H2O2). It has also been suggested that postischemic hyperoxia, e.g. an increased oxygen tension during the recirculation period, adversely affects recovery following transient ischemia. Other data support the notion that brain damage caused by permanent ischemia (stroke) is significantly influenced by production of free radicals. The present study, however, fails to show that recirculation following brief periods of ischemia (15 min) leads to an enhanced H2O2 production, and that hyperoxia aggravates the ischemic damage. This study was undertaken to reveal whether variations in oxygen supply in the postischemic period following forebrain ischemia in rats affect free radical production and the brain damage incurred. To that end, rats ventilated on N2O/O2 (70:30) were subjected to 15 min of transient ischemia. Normoxic animals were ventilated with the N2O/O2 mixture, hyperoxic animals with 100% O2, and hypoxic ones with about 10% O2 (balance either N2O/N2 or N2) during the recirculation. At the end of this period, the animals were decapitated for assessment of H2O2 production with the aminotriazole/catalase method. This method is based on the notion that aminotriazole interacts with H2O2 to inactivate catalase; thus, the rate of inactivation of catalase in aminotriazole treated animals reflects H2O2 production. In a parallel series, animals ventilated with one of the three gas mixtures in the early recirculation period, respectively, were allowed to recover for 7 days, with subsequent perfusion-fixation of brain tissues and light microscopical evaluation of the brain damage. Animals given aminotriazole, whether rendered ischemic or not, showed a reduced tissue catalase activity, reflecting H2O2 production in the brain. Hyperoxic animals failed to show increased tissue H2O2 production, while hypoxic ones showed a tendency towards decreased production. However, all three groups (hypo, normo- and hyperoxic) had similar density and distribution of neuronal damage. These results suggest that although postischemic oxygen tensions may determine the rates of H2O2 production, variations in oxygen tensions do not influence the final brain damage incurred.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Free radical production and ischemic brain damage: influence of postischemic oxygen tension. 205 15

Much of the research related to cardiopulmonary bypass in recent years has been directed toward defining the changes in plasma and blood cells during bypass. In this review, recent information is reexamined for six areas of current interest. These areas are complement activation, immune response, anaphylactic reactions, coagulation, and cerebral dysfunction. Complement may be activated by either the classical or alternate pathway during cardiopulmonary bypass and protamine administration. Membrane oxygenators appear to diminish the degree of complement activation. Complement is a major factor in the whole body inflammatory response; which often accompanies cardiopulmonary bypass. A product of complement activation, C5a- desArg, causes activation and aggregation of granulocytes. Other products of complement activation lead to lysis of blood cells including granulocytes and red cells. Bubble oxygenators appear to have a distinct disadvantage compared to membrane oxygenators regarding infection. Airborne microorganisms are more likely to be entrained into circulating blood with bubble oxygenators than with membrane oxygenators. Bubble oxygenators cause a greater decrease in leukocyte number and function than membrane oxygenators. Anaphylactic reactions have been associated with use of antibiotics, blood products, protamine, and volume expanders during cardiopulmonary bypass. Protamine reactions may be on an immunological basis or due to direct toxicity of the drug. Free radicals including superoxide, hydrogen peroxide, and the hydroxyl radical may be generated during cardiopulmonary bypass and reperfusion. Free radical scavengers including; vitamin E, coenzyme Q, vitamin C, mannitol, and glutathione have been studied. The avoidance of blood transfusion because of risk of transmitted infection including AIDS has become a major goal in cardiac surgery. Factors that correlate with increased transfusion requirement include low hematocrit, female gender, increased age, small body size, low ejection fraction, reoperation, and emergency operation. Heparin resistance due to antithrombin III deficiency is being recognized more commonly. Antithrombin III deficiency may be corrected with fresh frozen plasma. Patients with heparin induced thrombocytopenia may be difficult to manage. Several management protocols are suggested. The most straightforward appears to be the use of aspirin preoperatively and platelet transfusions postoperatively. The incidence of cerebral dysfunction after cardiopulmonary bypass depends on the sensitivity of the test or indicator used. Perioperative stroke is associated with intrinsic cerebrovascular disease and atherosclerosis of the ascending aorta. Retinal angiograms during cardiopulmonary bypass show that microemboli are very common. Cerebroplegia has been shown to extend the period of safe circulatory arrest in animals. Much of the new knowledge concerning cardiopulmonary bypass is the result of close collaboration between cardiac surgeons and nonsurgical scientists.
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PMID:Pathophysiology of cardiopulmonary bypass: current issues. 213 41

Leukocytes recruited to regions of focal cerebral ischemia may contribute to tissue injury by their ability to promote inflammation. A novel group of drugs, the 21-aminosteroids, have been observed to reduce neurologic damage and vasogenic cerebral edema in animal models of stroke by inhibiting lipid peroxidation. Production of hydrogen peroxide and free radicals by leukocytes during the inflammatory response may contribute to lipid peroxidation and other consequences of free radical-mediated tissue injury. We assessed the effect of U74500A, a 21-aminosteroid, on the generation of hydrogen peroxide by and on the chemiluminescence of stimulated polymorphonuclear leukocytes and monocytes from normal humans. U74500A significantly reduced the generation of hydrogen peroxide by polymorphonuclear leukocytes (p less than 0.001) and monocytes (p less than 0.01) in a dose-dependent manner. Monocyte chemiluminescence was also significantly inhibited (p less than 0.05), but polymorphonuclear leukocyte-associated chemiluminescence was unchanged. Our results indicate that U74500A can reduce the concentration of oxygen metabolites associated with stimulated human leukocytes, and this effect may explain in part how 21-aminosteroids reduce lipid peroxidation, ischemic injury, and vasogenic edema.
Stroke 1990 Oct
PMID:A 21-aminosteroid reduces hydrogen peroxide generation by and chemiluminescence of stimulated human leukocytes. 221 8


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