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Biomedical subjects

L Csiba

Publications and source records attributed to L Csiba.

62 records · Page 4Linked to original sources
PubMed1983

A topographic quantitative method for measuring brain tissue pH under physiological and pathophysiological conditions.

A technique was developed for the quantitative regional assessment of brain pH by a modification of the umbelliferone method. Twenty micron thick sections were brought into contact with umbelliferone-soaked paper strips and the fluorescence (450 nm) following excitation at 370 nm and 340 nm was recorded photographically. The 340 nm excitation image was subtracted from 370 nm picture, using a computerized image-processing system. Regional pH values were measured in rats and cats under normal and ischemic conditions.

Acid-Base Equilibrium↗
PubMedDate not supplied

Regional pH and electrolyte homeostasis of cat brain after prolonged ischemia.

Following prolonged cerebral ischemia, primary electrophysiological recovery may be followed by secondary deterioration of the recovery process. It has been suggested that the secondary deterioration is caused by "late" cytotoxic brain edema. To test this hypothesis, adult normothermic cats were submitted to 1 h complete cerebral ischemia followed by 3 and 6 h recirculation, respectively. Postischemic recovery of energy metabolism was imaged by ATP-induced bioluminescence, and regional tissue pH and electrolyte content was measured in regions with and without metabolic recovery. In areas with postischemic restitution of metabolic activity, sodium gradually rose from 338 +/- 17 to 488 +/- 28 mumol/g protein and calcium from 8.81 +/- 0.35 to 18.24 +/- 0.97 mumol/g protein. Tissue potassium content decreased from 761 +/- 12 to 676 +/- 19 mumol/g protein and magnesium from 46.8 +/- 0.8 to 36.3 +/- 1.1 mumol/g protein. Tissue pH rose from 7.09 +/- 0.04 to 7.31 +/- 0.13 and 7.26 +/- 0.17 after 3 and 6 h recirculation, respectively. In areas without metabolic recovery, electrolyte disturbances were even more pronounced and pH--after transient alkalization--fell to 6.82 +/- 0.12. These data demonstrate that during the later phase of postischemic recirculation, progressive disturbances of electrolyte homeostasis create a preedematous situation that has to be considered for preventing delayed postischemic complications.

Adenosine Triphosphate↗
PubMedDate not supplied

A novel method of macropathologic and arteriographic examination of carotid specimens obtained from autopsy.

Twenty carotid bifurcations were examined. During autopsy, carotid bifurcations were removed in toto. Unfixed carotids were ligated and cannulated for injection of an angiographic contrast medium followed by injection of a tissue-embedding medium at physiologic pressure and temperature. The carotid bifurcation was frozen and cut manually in 3-mm cross-sections. Photographs were then taken of every slice. Angiography, filling with tissue-embedding material, and sectioning were successful in all cases. In the macropathologic sections, the extent, configuration and location of atherosclerotic lesions could be identified.

Aged↗
PubMedDate not supplied

Screening for depressive symptoms in the acute phase of stroke.

Depressive symptoms can often be observed after stroke. We prospectively evaluated patients at a stroke unit in order to determine the occurrence and severity of depressive symptoms in the acute phase of stroke in 82 patients 7 +/- 2 days after admission to the stroke unit. Severity of stroke was evaluated by the Scandinavian and Orgogozo scales and the Barthel index. Severity of depressive symptoms was measured by the 13-item Beck scale. Mean age of the patients was 65.8 years. No gender difference was observed in the severity of stroke or depressive symptoms. DSM-IV criteria of adjustment disorder with depressed mood were fulfilled by 27% of the patients. In this group, stroke was significantly more severe by the Barthel, Orgogozo, and Scandinavian scales (p < 0.001). Whereas Beck score was at least 10 in 19.5%, severe depressive symptoms (Beck score > or = 15) occurred in less than 5% of patients with acute stroke. Those who could not walk by themselves or who were aphasic had significantly higher mean Beck scores (6.3 +/- 5.1 vs 2.4 +/- 3.1, p < 0.001, and 7.0 +/- 5.8 vs 3.4 +/- 3.9, p = 0.002). Significant correlation was found between the severity of stroke and that of the depressive symptoms (r = -0.56, -0.58, and -0.54 for the Scandinavian, Orgogozo, and Barthel scales, p < 0.001).

Activities of Daily Living↗
PubMedDate not supplied

Cerebrovascular reactivity and reserve capacity in type II diabetes mellitus.

The aim of the study was to test the hypothesis that cerebrovascular reserve capacity and cerebrovascular reactivity are impaired in patients suffering from non insulin-dependent diabetes mellitus. We also intended to investigate factors which may influence resting cerebral blood flow velocity and cerebrovascular reserve capacity. A total of 28 patients suffering from type II diabetes mellitus and 20 healthy control subjects were studied. Based on diabetes duration patients were divided into two groups: subjects with > 10 years and those with < or = 10 years disease duration. Middle cerebral artery mean blood flow velocities were measured at rest and after intravenous administration of 1g acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated. Blood glucose, insulin, glycosylated hemoglobin, hemostatic factors (fibrinogen, alpha-2 macroglobulin and von Willebrand factor antigen) were determined. Cerebrovascular reactivity and reserve capacity values were compared between the two diabetic subgroups and controls. Correlations between laboratory parameters and cerebrovascular reserve were investigated by linear regression analysis. Resting cerebral blood flow velocity was similar in controls and in the two diabetic subgroups. Cerebrovascular reactivity was elevated for a shorter time in patients with > 10 years disease duration than in controls and short-term diabetic patients. Cerebrovascular reserve capacity was lower in the long-term diabetes group (means +/- SD: 39.6 +/- 20.7%) than in patients with < or = 10 years disease duration (63.3 +/- 17.4%, p < 0.02 after Bonferroni correction). Cerebrovascular reserve capacity was inversely related to the duration of the disease (R = 0.53, p < 0.003). None of the determined laboratory factors had any relation with resting cerebral blood flow and cerebrovascular reserve capacity. The vasodilatory ability of cerebral arterioles is diminished in long-standing type II diabetes mellitus.

Aged↗
PubMedDate not supplied

Cations of cisternal cerebrospinal fluid in humans and the effect of different doses of nimodipine on CSF calcium after stroke.

Cisternal samples of cerebrospinal fluid (CSF) were analyzed for protein, albumin, sodium (Na), potassium (K), and calcium (Ca) content in 21 control subjects and 64 patients who had experienced acute stroke. A second cisternal CSF sample was taken in 37 of the stroke patients after 2-3 weeks treatment with the calcium antagonist nimodipine. Increased permeability of the blood-brain barrier was reflected by the significantly higher CSF/serum ratio of albumin in stroke patients than in control subjects (0.0046 vs. 0.0028,p = 0.0012). Serum and CSF concentrations of Na, K, and Ca did not differ between control subjects and stroke patients. In control subjects and in stroke patients, concentration of calcium in cisternal CSF ([Ca]) was smaller than values reported by others in lumbar samples. In stroke patients, the pH of CSF was lower than that of simultaneously taken blood (7.38 vs. 7.44, p < 0.001). No differences between stroke patients and control subjects were found for the cisternal CSF/serum ratios of Na (1.0 and 0.99), K (0.61 and 0.63), and Ca (0.25 and 0.24). When patients and controls were pooled together, CSF total [Ca] correlated weakly with serum total [Ca] (Spearman r = 0.28, p = 0.014) and with serum ionized [Ca] (Spearman r = 0.27, p = 0.016). After 2-3 weeks of nimodipine treatment, CSF [Ca] was significantly lower in the subgroup treated with 60 mg nimodipine four times daily (240 mg/d) than with 30 mg four times daily. A nimodipine dosage of 30 mg four times daily (120 mg/d) did not affect CSF [Ca]. A 240 mg daily dosage, but not a 120 mg daily dosage, of nimodipine may affect the Ca transport system in humans at the choroid plexus.

Acute Disease↗
PubMedDate not supplied

Monocytes express tissue factor in young patients with cerebral ischemia.

Activation of blood coagulation and fibrinolysis has previously been detected in stroke patients. It is unknown, however, what factors contribute to the acceleration of coagulation reactions, especially in cases where no obvious predisposing factors exist. We therefore postulated and tested the hypothesis that in such patients monocytes may trigger the pathway leading to thrombosis by expressing tissue factor (TF). TF antigen was determined in 48 patients and 40 controls by flow cytometry using an indirect immunofluorescent technique. TF antigen expression was significantly increased on monocytes in young stroke patients in both the acute (p < 0.01) and chronic (p < 0.05) phases of the disease. The TF antigen also possessed functional activity, quantitated by a one-stage clotting assay. TF expression on monocytes was not associated with an elevation in C-reactive protein values. In both acute and chronic phases, blood coagulation activation markers, e.g. the thrombin-antithrombin complex and F1 + 2 fragments, were significantly elevated. However, in the acute phase D-dimer levels were similar to those in controls and were only elevated in the chronic phase of the disease (p < 0.05). In conclusion, in cerebral ischemia TF expression on monocytes suggests enhanced activation of blood coagulation and subsequent fibrinolysis.

Adolescent↗