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Biomedical subjects

I Fekete

Publications and source records attributed to I Fekete.

At least 19 recordsLinked to original sources
PubMed1996

[Low doses of acetylsalicylic acid effectively inhibits thrombocyte aggregation after ischemic stroke].

Platelet aggregation was examined in 43 patients after ischemic stroke and in 16 healthy subjects using multiparametric aggregation index (MAI). The value of MAI was significantly higher in stroke patients (3.15 in patients and 0.92 l/mumol in controls, p < 0.0001). Patients who had increased MAI (n = 26) were treated with a daily dose of 100 mg acetilsalicylic acid (ASA). Platelet activity was measured before and on the 7th and 28th day of treatment measuring three parameters: MAI, spontaneous dysaggregation and collagen induced aggregation. All 3 methods showed a significant decrease in platelet aggregation on the 7th day of treatment, but further changes were not found on the 28th day. Serum levels of thromboxane-A2 (TXA2) and prostacycline (PGI2) metabolites (TXB2 and 6-keto-prostaglandin-F1 alpha) were determined before and on the 28th day of treatment. The effect of 100 mg ASA per day proved to be selective: comparing the serum levels before and after treatment, a significant decrease of TXB2 concentration was found without changes in the concentration of 6-keto-prostaglandin-F1 alpha. Evaluating MAI and the value of dysaggregation might reflect ineffectiveness of antiplatelet therapy in patients not responding to a daily dose of 100 mg of ASA. For these patients the increase of the daily dose of ASA, or changing to another antiplatelet drug might be recommended.

Aged↗
PubMed1995

Beneficial vascular and metabolic effects of cobalt-ATP in spontaneously hypertensive rabbits with diffuse chronic cerebral ischaemia.

The in vivo effects of adenosine triphosphate (ATP) have not been investigated in cerebrovascular diseases. The use of the long-acting cobalt-ATP complex (Co-ATP) permits us to observe the effects of ATP without the influence of its metabolites. This study was designed to compare the effects of intravenous Co-ATP on the cerebral blood flow (CBF), polarographically detected oxygen currents (O2a), mean arterial blood pressure (MABP), heart rate, respiration rate, cerebral electrical activity, arterial blood gases, pH, and glucose in 13 normotensive (NT) rabbits to those in 14 stroke-prone spontaneously hypertensive (HT) animals. CBF was measured by the hydrogen and heat clearance methods. In response to Co-ATP, MABP decreased and CBF increased significantly in both groups. The decrease in MABP was more marked in HT rabbits, while CBF response was 25% smaller than in NT animals. The ratio of O2a to CBF diminished moderately and simultaneously with the CBF increase in NT rabbits. In HT rabbits, the decrease in O2a/CBF was larger and began when CBF response reached its maximum. We suggest that despite the restricted CBF response, long-acting ATP should still be taken into consideration as a supplementary treatment of hypertensive encephalopathy because of its beneficial effects on cerebral metabolism and hypertension.

Adenosine Triphosphate↗
PubMed1995

[Excretion of cefonicid and ceftriaxone into the saliva].

The serum and saliva levels of cefonicid (Monocid) and ceftriaxon (Rocephin) were studied after iv. administration on mice. It was found that both of the antibiotics were secreted well into saliva and their therapeutic values remained for 4-5 hours.

Animals↗
PubMed1995

[Excretion of fluoroquinolones into saliva].

The excretion of three fluoroquinolones derivatives into the saliva were studied in animal experiments. Ofloxacin per os administered to rabbits was excreted into the saliva well, and maintained the therapeutic level long--about 7 hours. Pefloxacin and ciprofloxacin iv. administered to mice were similarly excreted into the saliva at therapeutic levels and retained the antibacterial level for about 4 hours.

Animals↗
PubMed1994

Increased proportion of docosahexanoic acid and high lipid peroxidation capacity in erythrocytes of stroke patients.

BACKGROUND AND PURPOSE: Intracellular accumulation of lipid peroxides that derive from the autoxidation of membrane polyunsaturated fatty acids reduces the deformability of erythrocytes contributing to the hemorheological disturbances observed in acute cerebral ischemia. The present study deals with the biochemical background of increased lipid peroxidation capacity in the erythrocytes of stroke patients. METHODS: A complete clinical and laboratory assessment was made of 24 men and 18 women (aged 50 to 78 years; 64.5 +/- 13.9 years, mean +/- SD) who had an ischemic hemispheric lesion of the brain. Lipid peroxide content, lipid peroxidation capacity, superoxide dismutase activity, and fatty acid composition of erythrocytes were compared in stroke patients and 22 healthy subjects matched for age. The lipid peroxide content of the erythrocytes was estimated before and after the autoxidative test; the results were expressed as nanomoles of malondialdehyde per gram of hemoglobin. The increase of the lipid peroxide content in the erythrocytes during the autoxidative test measures the lipid peroxidation capacity. RESULTS: In comparison with healthy subjects (1.45 +/- 0.30 nmol MDA/g Hb per 24 hours), the lipid peroxidation capacity was found to be significantly higher (4.18 +/- 0.41 nmol MDA/g Hb per 24 hours) (P < .01) in the erythrocytes of stroke patients. The stroke patients could be divided into two groups on the basis of lipid peroxidation capacity of their erythrocytes. Twenty patients had erythrocytes with high lipid peroxidation (< 4 nmol MDA/g Hb per 24 hours), and 22 patients had very high lipid peroxidation capacity (> 4 nmol MDA/g Hb per 24 hours). There was no significant difference in superoxide dismutase activity in the erythrocytes of patients compared with healthy subjects. Before the autoxidative test was conducted, the fatty acid composition in the erythrocytes of stroke patients with very high lipid peroxidation capacity was measured and found to be generally normal; only the proportion of docosahexanoic acid (22:6 n-3) was markedly (P < .01) increased. CONCLUSIONS: The results suggest that the erythrocytes of ischemic stroke patients with very high lipid peroxidation capacity displaying an abnormal fatty acid composition are much more vulnerable to lipid peroxidation. The increased proportion of docosahexanoic acid and the high lipid peroxidation capacity of erythrocytes play a pathogenetic role and explain the hemorheological disturbances observed in the microcirculation of stroke patients.

Aged↗
PubMed1993

Effects of dipyridamole in spontaneously hypertensive rabbits with diffuse chronic cerebral ischemia.

The effect of intravenous dipyridamole (0.7 mg/kg) on cerebral blood flow (CBF), mean arterial blood pressure (MABP), heart rate, respiration rate, cerebral electrical activity, arterial blood gases, pH, and glucose was investigated in 14 normotensive and 14 stroke-prone spontaneously hypertensive anesthetized rabbits. CBF was measured by hydrogen and heat clearance. In both groups, MABP decreased (normotensive: -24 mm Hg, hypertensive: -47 mm Hg; ANOVA: P < 0.0001) and CBF increased (normotensive: +59 ml/100 g/min, hypertensive: +72 ml/100 g/min; ANOVA: P < 0.0002). CBF returned to the initial level 21 min later in hypertensive than in normotensive rabbits. Changes in other parameters were insignificant. In additional experiments, 30 mg/kg theophylline entirely prevented the cerebral vasodilator and systemic hypotensive effects of dipyridamole in both normotensive and hypertensive rabbits. We conclude that, in stroke-prone spontaneously hypertensive rabbits, the longer-lasting and larger CBF increase in response to dipyridamole may be attributed to reversible functional changes in the cerebral vasculature resulting from hypertension.

Analysis of Variance↗
PubMed1992

The effect of an amino acid-lowering diet on the rate of melphalan entry into brain and xenotransplanted glioma.

Melphalan (L-phenylalanine mustard, L-PAM, alkeran; molecular weight, 305,000) is transported across tumor cell membranes and the blood-brain barrier by the large neutral amino acid (LNAA) transport system. Normally, plasma LNAA levels are high enough and the affinity low enough that this system does not transport much melphalan into the brain. However, plasma amino acids can be reduced by fasting and protein-free diet. We used this method to reduce competition and to increase melphalan transport into brain tumors. In nude mice fasted for 12 h and then fed a protein-free diet for 2 and 6 h, mean plasma LNAA levels were 46% and 42% of control values. Nude mice with xenotransplanted D-54MG human gliomas were used to study tissue distribution and uptake kinetics of [3H]melphalan in a control group and a diet group (after a 12-h fast and 2 h of a 0% protein diet). The K1 (blood-to-tissue transfer constant) of melphalan, determined by graphical analysis and by nonlinear fitting to a 2-compartment model, was higher in the diet group in all tumor regions except the necrotic center of subcutaneous tumors; the increase was significant in the tumor periphery of brain and s.c. tumors. The ratio of K1s (diet to control) varied from 1.2 to 1.3 in brain tumors, 1.9 to 2.1 in subcutaneous tumors, and 1.8 to 3.1 in tumor-free brain. The apparent [3H]melphalan distribution space was significantly higher in the tumor periphery of both brain and subcutaneous tumors of the 15- and 30-min diet group. We also measured blood-brain barrier transport of [alpha-14C]aminoisobutyric acid and blood flow (with [131I]iodoantipyrine): the K1 of [alpha-14C]aminoisobutyric acid was 28.1 +/- 6.6 (SE) in brain tumors and 24.3 +/- 8.9 microliters/g/min in subcutaneous tumors. Blood flow was 58.2 --> 3.9 in brain tumors and 5.2 +/- 0.4 ml/100 g/min in subcutaneous tumors. Fasting, when combined with a protein-free diet, reduces plasma amino acid levels and thereby reduces competition between melphalan and LNAAs. This may increase the amount of melphalan that can enter a brain tumor without increasing the administered drug dose and suggests a therapeutic manipulation that can be used to increase the delivery of melphalan.

Amino Acid Transport Systems↗
PubMed1992

Effects of carbon dioxide inhalation on cerebral blood flow and oxygen tissue level in spontaneously hypertensive rabbits.

BACKGROUND AND PURPOSE: Because previous studies have yielded conflicting results, this study was designed to investigate the efficiency of cerebrovascular reactivity to carbon dioxide in hypertension associated with moderate diffuse cerebral ischemic lesions. METHODS: The effects of carbon dioxide inhalation on mean arterial blood pressure, heart and respiration rates, cerebral cortical blood flow, polarographically detected oxygen currents (oxygen availability), and cerebral electrical activity were compared in 14 spontaneously hypertensive and 16 normotensive rabbits anesthetized with urethane and alpha-chloralose. Blood flow was measured with the hydrogen clearance and thermal clearance methods. RESULTS: In the resting state the frequency of electrical activity shifted to slower components, the levels of oxygen availability and cerebral blood flow were lower (p less than 0.01), and the ratio of the two latter parameters was greater (p less than 0.01) in hypertensive rabbits than in normotensive animals. Carbon dioxide inhalation induced more marked increases in cerebral blood flow, respiration rate, and oxygen availability in hypertensive (p less than 0.01) than in normotensive (p less than 0.05) rabbits. The ratio of oxygen availability to cerebral blood flow decreased (p less than 0.01) in the former and did not change significantly in the latter group. The carbon dioxide-induced rise in blood flow was also slower and more protracted in hypertensive rabbits (p less than 0.01). Histological investigation revealed groups of neurons with ischemic changes in the cortex of the hypertensive rabbits. CONCLUSIONS: We suggest that in hypertensive rabbits the mild multiple ischemic lesions are the basis of functional disturbances, including reduced resting cerebral blood flow, greater oxygen tissue level, slower response to carbon dioxide, and greater vasodilatory capacity.

Administration, Inhalation↗
PubMed1991

Difference between the cerebrovascular effect of purinergic Co-ATP and that of the cholinesterase inhibitor, physostigmine, in vivo.

Development of the cerebrovascular effect of cobalt-ATP was compared to that of physostigmine in 34 anesthetized rabbits. The resting cortical cerebral blood flow (CBF) was estimated from the H2 clearance and the CBF changes by the heat clearance method. Systemic blood pressure, heart and respiratory rate and cerebral electrical activity were recorded simultaneously. In addition, we measured arterial glucose concentration, pH, PaO2 and PaCO2. Both drugs were found to induce a significant increase in CBF. However, the degree of the CBF increase induced by Co-ATP was inversely related, while that induced by physostigmine was directly related to both the baseline level of CBF and the value of PaCO2. We conclude that the cerebrovascular effect of ATP depends mainly on vessel tone, while the effect of physostigmine is related to the level of PaCO2.

Adenosine Triphosphate↗
PubMed1990

Rate of buthionine sulfoximine entry into brain and xenotransplanted human gliomas.

Buthionine sulfoximine (BSO) is an inhibitor of glutathione synthesis and can be used to potentiate the effects of chemotherapeutic alkylating agents and radiotherapy. We examined the rates of influx and efflux of [35S]BSO administered to athymic mice with and without xenografted D-54MG human gliomas. Three analytic approaches were applied to the experimental data to obtain values of the blood-to-tissue influx constant, K1, of BSO. Multiple time point experiments in tumor-bearing mice were analyzed with a two-compartment model and nonlinear fitting routines, and by graphical analysis which assumed no backflux of BSO from tissue to blood. A third approach used single time point data in nontumor-bearing mice and assumed no backflux. Calculated values of the K1 of BSO ranged from 0.23 to 1.35 microliters/g/min in tumor-free cortex, and from 5.3 to 6.3 microliters/g/min in the D-54MG gliomas. The tissue-to-blood efflux constant, k2, was zero in both cortex and tumor, suggesting that BSO entered cells and was trapped once it crossed the blood-brain barrier. Estimates of plasma vascular space (Vp) ranged from 2 to 20 microliters/g in cortex, and from 103 to 169 microliters/g in tumor. Another set of experiments, done in normal mice with different doses of BSO, suggested that BSO competes for neutral amino acid transport sites at the blood-brain barrier, but that the capacity of the carrier-mediated transport system is low and saturates at administered doses of about 0.5 mmol/kg (corresponding to plasma concentrations of about 12 mumol/ml). The rate of entry into brain was proportional to the octanol/water partition coefficient and molecular weight of BSO, which also supports passive diffusion as the means of entry. Consequently, although the rate of BSO entry into D-54MG gliomas was between 4 and 30 times higher than the rate of entry into tumor-free cortex, the results of these experiments suggest that most of the BSO that enters brain tumors in the doses commonly used in experimental situations will cross capillaries by passive diffusion.

Animals↗
PubMed1990

[Significance of computer analysis of dynamic brain scintigraphy in patients with cerebrovascular disorders].

Dynamic cerebral scintigraphy was performed on 41 patients with cerebrovascular disease. The diagnostic value of parametric images formed by a computer was correlated to angiographic findings and clinical sings, respectively. Having the appropriate software these examinations can be performed with traditional gamma-cameras. Analysis of parametric pictures increases the reliability of the method. Analysis of cinematic display of serial images had the highest sensitivity and accuracy, while time-of-maximum pictures had the highest specificity. In departments, where digitized subtraction angiography, single photon emission computed tomography or positron emission tomography is not available, the non invasive dynamic brain scintigraphy is a useful screening method, its application is proposed by the authors.

Adolescent↗
PubMed1988

Cerebral ischaemia produced by homologous blood clot emboli in rabbit.

In 40 rabbits cerebral ischaemia was induced by autologous blood clot emboli injected into the middle cerebral artery. Autologous blood clot formed spontaneously (within 2 h) in a catheter fixed in the internal carotid artery. The effects of embolization were investigated on arterial blood pressure, respiration, local cerebral blood flow, locally available O2 (aO2), steady (DC) potentials and EEG. After embolization the blood pressure and the frequency of respiration decreased transiently. On the embolized side the local cerebral blood flow, aO2, the frequency and amplitude of the EEG diminished markedly and the DC potentials shifted to negative. Similar but less marked and short-lasting changes could be seen on the contralateral side. Pathological examination of the brains revealed extensive infarction with haemorrhagic components. The technique is a promising method for inducing stroke experimentally and offers various ways for its thorough investigation.

Animals↗
PubMed1988

A new model for inducing transient cerebral ischemia and subsequent reperfusion in rabbits without craniectomy.

An artificial ball removable by an attached fiber was injected into the middle cerebral artery (MCA) of 16 rabbits, allowing the study of transient (5, 10, 15, or 30 minutes) cerebral ischemia without craniectomy. Measurements of available oxygen (aO2) in the ischemic core (the ventral part of the temporal area) followed by histologic examination verified the embolization. Electroencephalographic power spectra and steady (direct current) potentials were recorded bilaterally on the convexity remote from the actual lesion but still supplied by the MCA. Local cerebral blood flow and aO2 in the border zone between the anterior cerebral artery and the occluded MCA were measured. Embolization caused typical ischemic changes ipsilaterally and alterations characteristic of diaschisis contralaterally. Extreme border zone hyperemia developed without significant aO2 changes in the same region. Restoration of circulation via the circle of Willis induced gradual normalization. Our model for controlled embolization and recirculation proved suitable for detailed studies of the complex changes in brain function caused by transient ischemia.

Animals↗
PubMed1985

Experimental focal cerebral ischaemia in rabbits.

A highly reproducible form of experimental embolization of the intracranial arteries is presented in rabbits. The injection of a silver or gold ball into the internal carotid artery caused occlusion predominantly of the middle cerebral artery and/or its branches. At the moment when embolization took place, the characteristic signs of acute cerebral ischaemia occurred in the electroencephalogram, local cerebral blood flow and steady (DC) potentials. Several hours after the ball had been injected the extent of the focal lesions became recognizable on sections stained for myelin. The procedure is simple, rapid, inexpensive and practically always successful. The extent of the lesion may be influenced by the change of both the ball size and the posture of animals. Moreover, the site of occlusion is easily discernible both on radiographs and to the naked eye.

Animals↗
PubMed1984

Case report of infarction in the region of the posterior spinal arteries.

Spinal cord infarction in the region of the posterior spinal arteries is reported in a 62-year-old woman. The softening was restricted to the lumbosacral region involving two segments. Sectioning the affected and adjacent segments serially no occlusion was found in the posterior spinal arteries. Besides the circumscribed infarction the microscopic picture of the spinal cord was characteristic of vascular myelopathy. The underlying disorders of the previously reported cases and the predisposing factors contributing to the development of infarction are discussed. It is concluded that an insufficient anastomotic network plays the essential role in the pathogenesis of the spinal cord infarction.

Arteries↗