The aim of the present study was to evaluate the efficiency of combination of hyperbaric oxygen (HBO) and an antioxidant on permanent focal cerebral ischemia. Male Wistar rats underwent permanent middle cerebral artery occlusion (MCAO). Then, animals were randomly assigned to one of four groups: the control group (n=9) received no treatment, HBO group (n=9) was treated for 90 min at 2.5 absolute atmosphere for 3 days, the U-74389G group (n=8) received single U-74389G injection (3 mg/kg), the HBO + U-74389G group (n=8 ) received both HBO and U-74389G treatments. Treatments were initiated within the first 10 min after MCAO. After 3 days, the infarct volumes in rat brains were measured. The infarct ratios were 25.6±6.5 % for the control group, 21.9±6.4 % for the HBO group, 15.7±5.7 % for U-74389G group and 12.5±3.8 % for HBO + U74389G group. The infarct volumes were significantly reduced in rats treated with U-74389G (p< 0.05) and combination therapy (p <0.05). HBO failed to reduce infarct volume significantly. We concluded that 1) U-74389G is more beneficial than HBO on permanent MCAO in rats, and 2) a combined therapy failed to significantly improve infarct volume more than either single treatment., G. Acka, A. Sen, Z. Canakci, S. Yildiz, A. Akin, G. Uzun, H. Cermik, I. Yildirim, S. Kokpinar., and Obsahuje bibliografii a bibliografické odkazy
The objective of this study was to evaluate the effect of diet and 677 C®T mutation of the methylenetetrahydrofolate reductase (MTHFR) gene on plasma homocyst(e)ine concentrations in an adolescent population (113 males, age: 14.2±2.4 years; 202 females, age: 14.9±2.1 years) from a region characterized by high cardiovascular mortality. Homocyst(e)ine levels did not differ between males and females (9.4±3.5 and 8.9±3.1 mmol/l, respectively). The homozygosity for the 677 C®T MTHFR mutation was found in 4.6 % of subjects. No differences in homocyst(e)ine levels were found between MTHFR genotypes. Analysis of the diet composition which was performed on a 24-hour daily recall basis and a food frequency questionnaire showed a low daily intake of vitamin B6 (males: 1.13 mg/66 % RDA; females: 0.92 mg/61 % RDA). Daily folic acid intake was 0.21 g/105 % RDA in males and 0.23 g/115 % RDA in females. The results of our study show that the high homocyst(e)ine levels in the adolescent population were not affected by the 677 C®T MTHFR mutation. We conclude that an insufficient dietary intake of vitamin B6 and folic acid is responsible for this finding. This is in accord with the recommendation that the dietary allowances for folate should be reset to the originally prescribed levels of 0.4 g/day which should be sufficient to control the homocysteine levels., K. Rašlová, A. Bederová, J. Gašparovič, P. Blažíček, B. Smolková., and Obsahuje bibliografii
a1_The effect of different muscle shortening velocity was studied during cycling at a pedalling rate of 60 and 120 rev.min-1 on the [K+]v in 21 healthy young men (aged 22.5±2.2 years, body mass 72.7±6.4 kg, VO2max 3.720±0.426 l . min-1) performing an incremental exercise test until exhaustion. The power output increased by 30 W every 3 min, using an electrically controlled ergometer Ergoline 800S (see Zoladz et al. J. Physiol. 488: 211-217, 1995). The test was performed twice: once at a cycling frequency of 60 rev.min-1 (test A) and a few days later at frequency of 120 rev.min-1 (test B). At rest and at the end of each step (i.e. the last 15 s) antecubital venous blood samples for [K+]v were taken. Gas exchange variables were measured continuously (breath-by-breath) using Oxycon Champion Jaeger. The pre-exercise [K+]v in both tests was not significantly different amounting to 4.24±0.36 mmol.l-1 in test A, and 4.37±0.45 mmol.l-1 in test B. However, the [K+]v during cycling at 120 rev.min-1 was significantly higher (p<0.001, ANOVA for repeated measurements) at each power output when compared to cycling at 60 rev.min-1. The maximal power output reached 293±31 W in test A which was significantly higher (p<0.001) than in test B, which amounted to 223±40 W. The VO2max values in both tests reached 3.720±0.426 l.min-1 vs 3.777±0.514 l.min-1. These values were not significantly different. When the [K+]v was measured during incremental cycling exercise, a linear increase in [K+]v was observed in both tests. However, a significant (p<0.05) upward shift in the [K+]v and a % VO2max relationship was detected during cycling at 120 rev.min-1. The [K+]v measured at the VO2max level in tests A and B amounted to 6.00±0.47 mmol.l-1 vs 6.04±0.41 mmol.l-1, respectively., a2_This difference was not significant. It can thus be concluded that a) generation of the same external mechanical power output during cycling at a pedaling rate of 120 rev.min-1 causes significantly higher [K+]v changes than when cycling at 60 rev.min-1, b) the increase of venous plasma potassium concentration during dynamic incremental exercise is linearly related to the metabolic cost of work expressed by the percentage of VO2max (increase as reported previously by Vollestad et al. J. Physiol. Lond. 475: 359-368, 1994), c) there is a tendency towards upward shift in the [K+]v and % VO2max relation during cycling at 120 rev.min-1 when compared to cycling at 60 rev.min-1., J. A. Zoladz, K. Duda, J. Majerczak, P. Thor., and Obsahuje bibliografii
We examined the effect of ethanol on single potassium channels derived from plasma membranes of bovine tracheal smooth muscles. The observed potassium channels had a conductance of 296±31 pS (mean ± S.D.) in symmetrical 250 mmol/l KCl solutions, and exhibited a voltage- and Ca2+-dependence similar to BKCa channels. Ethanol at 50, 100 and 200 mM concentrations increased the probability of open potassium channels to 112±5, 127±7 and 121±13% (mean ± S.E.M.), respectively. It is suggested that increased activity of the BKCa channels by ethanol hyperpolarizes the plasma membrane and thus may contribute to relaxation of tracheal smooth muscle., V. Komínková, M. Magová, A. Mojžišová, Ľ. Máleková, K. Ondriaš., and Obsahuje bibliografii
The cornerstone of cardiovascular risk management is lifestyle intervention including exercise which could exert favorable impact also in renal transplant recipients. Nevertheless, reliable assessment of the effect of lifestyle interventions is complicated and the available data in this population are not consistent. The aim of the study was to evaluate the effect of physical activity on selected laboratory markers of vascular health including circulating stem cells, endothelial progenitor cells, microparticles, and plasma asymmetric dimethyl arginine in renal transplant recipients. Nineteen men and 7 women were recruited in 6-month program of standardized and supervised exercise. Control group consisted of 23 men and 13 women of similar age and body mass i ndex not included into the program. One year after the transplantation, the main difference between intervention and control group was found in the change of endothelial progenitor cells (p=0.006). Surprisingly, more favorable change was seen in the contro l group in which endothelial progenitor cells significantly increased compared to the intervention group. The explanation of this finding might be a chronic activation of reparative mechanisms of vascular system in the population exposed to multiple risk factors which is expressed as relatively increased number of endothelial progenitor cells. Therefore, their decrease induced by exercise might reflect stabilization of these processes., J. Piťha, I. Králová Lesná, P. Stávek, A. Mahrová, J. Racek, A. Sekerková, V. Teplan, M. Štollová., and Obsahuje bibliografii
a1_In the present work the effects of fasting and refeeding on fat pad weight and alkaline phosphatase activity in the brush border of individual duodenal enterocytes have been evaluated in male Wistar rats with obesity induced by monosodium glutamate (MSG) treatment during the early postnatal period. Neonatal rats were treated subcutaneously with MSG (2 mg/g b.w.) or saline (controls) for 4 days after birth. At 4 months of age, two types of experiments were performed. In the first experiment rats, were submitted to 3 or 6 days lasting food deprivation. In the second experiment the rats were refed for 3 or 6 days ad libitum or restrictedly (60 % of pre-fasting intake) after a 6 day-fasting period. Fasting and refeeding influenced the body fat and function of the duodenum in MSG-treated rats differently as compared to the controls. However, alkaline phosphatase activity and the weight of epididymal and retroperitoneal fat depots were significantly increased in MSG obese rats (P<0.001) during all the periods examined. While 3 days of food deprivation resulted in both groups in a similar loss of adipose tissue weight and alkaline phosphatase activity, the decrements of these parameters after 6 days of fasting were lower in obese rats suggesting that their capacity to spare body fat stores was enhanced. After 3 days of ad libitum refeeding, a more marked adaptational increase of food consumption and also a significantly increased alkaline phosphatase activity above the pre-fasting level (P<0.01) was observed in the MSG-treated rats. Consequently, a more rapid body fat restoration was demonstrated in these animals. Refeeding of rats at 60 % of the pre-fasting intake level resulted in a significant increase of alkaline phosphatase activity in both the MSG and control group; moreover, as food restriction continued, MSG-treated rats tended to further increase the enzyme activity., a2_Our results revealed that MSG treatment of neonatal rats may significantly change the intestinal functions. Permanently increased alkaline phosphatase activity observed in MSG obese rats during all investigated periods suggests that this functional alteration is probably not a consequence of actual nutritional variation but could be a component of regulatory mechanisms maintaining their obesity at critical values., Ľ. Raček, Ľ. Lenhardt, Š. Mozeš., and Obsahuje bibliografii
Intrauterine and perinatal life are critical periods for programming of cardiometabolic diseases. However, their relative role remains controversial. We aimed to assess, at weaning, sexdependent alterations induced by fetal or postnatal nutritional interventions on key organs for metabolic and cardiovascular control. Fetal undernutrition was induced by dam food restriction (50 % from mid-gestation to delivery) returning to ad libitum throughout lactation (Maternal Undernutrition, MUN, 12 pups/litter). Postnatal overfeeding (POF) was induced by litter size reduction from normally fed dams (4 pups/litter). Compared to control, female and male MUN offspring exhibited: 1) low birth weight and accelerated growth, reaching similar weight and tibial length by weaning, 2) increased glycemia, liver and white fat weights; 3) increased ventricular weight and tendency to reduced kidney weight (males only). Female and male POF offspring showed: 1) accelerated growth; 2) increased glycemia, liver and white fat weights; 3) unchanged heart and kidney weights. In conclusion, postnatal accelerated growth, with or without fetal undernutrition, induces early alterations relevant for metabolic disease programming, while fetal undernutrition is required for heart abnormalities. The progression of cardiac alterations and their role on hypertension development needs to be evaluated. The similarities between sexes in pre-pubertal rats suggest a role of sex-hormones in female protection against programming., D. Muñon-Valverde, P. Rodríguez-Rodríguez, P. Y. Gutierrez-Arzapalo, A. L. López de Pablo, M. Carmen González, R. López-Giménez, B. Somoza, S. M. Arribas., and Obsahuje bibliografii
Activation of GABAB receptors leads to longer inhibitory postsynaptic potentials than activation of GABAA receptors. Therefore GABAB receptors may be a target for anticonvulsant therapy. The present study examined possible effects of GABAB receptor agonist SKF97541 on cortical and hippocampal epileptic afterdischarges (ADs). Epileptic ADs elicited by electrical stimulation of sensorimotor cortex or dorsal hippocampus were studied in adult male Wistar rats. Stimulation series were applied 6 times with 10- or 20-min interval. Either interval was efficient for reliable elicitation of cortical ADs but stimulation at 10-min intervals did not reliably elicit hippocampal ADs, many stimulations were without effect. SKF97541 in dose 1 mg/kg significantly prolonged cortical ADs. Duration of hippocampal ADs was not significantly changed by either dose of SKF97541 in spite of a marked myorelaxant effect of the higher dose. Our present data demonstrated that neither cortical nor hippocampal ADs in adult rats were suppressed by GABAB receptor agonist SKF97541. Proconvulsant effect on cortical ADs indicates a different role in these two brain structures. In addition, duration of refractory period for electrically-induced ADs in these two structures in adult rats is different., P. Fábera, P. Mares., and Obsahuje bibliografii
The role of neuroendocrine responsiveness in the development of orthostatic intolerance after bed rest was studied in physically fit subjects. Head-down bed-rest (HDBR, -6 degrees, 4 days) was performed in 15 men after 6 weeks of aerobic training. The standing test was performed before, after training and on day 4 of the HDBR. Orthostatic intolerance was observed in one subject before and after training. The blood pressure response after training was enhanced (mean BP increments 18±2 vs. 13±2 mm Hg, p<0.05, means ± S.E.M.), although noradrenaline response was diminished (1.38±0.18 vs. 2.76±0.25 mol.l-1, p<0.01). Orthostatic intolerance after HDBR was observed in 10 subjects, the BP response was blunted, and noradrenaline as well as plasma renin activity (PRA) responses were augmented (NA 3.10±0.33 mol.l-1, p<0.001; PRA 2.98±1.12 vs. 0.85±0.15 ng.ml-1, p<0.05). Plasma noradrenaline, adrenaline and aldosterone responses in orthostatic intolerant subjects were similar to the tolerant group. We conclude that six weeks of training attenuated the sympathetic response to standing and had no effect on the orthostatic tolerance. In orthostatic intolerance the BP response induced by subsequent HDBR was absent despite an enhanced sympathetic response., J. Koška, L. Kšinantová, R. Kvetňanský, M. Marko, D. Hamar, M. Vigaš, R. Hatala., and Obsahuje bibliografii
Several neurodegenerative conditions, such as Alzheimer’s disease and Parkinson’s disease, or vascular dementia and cognitive impairment, are associated with mild hyperhomocysteinemia. Hyperhomocysteinemia is defined as an increas e of the homocysteine (Hcy) level beyond 10 μM. Although the adverse effect of Hcy on neurons is well documented, knowledge about the impact of this amino acid on glial cells is missing. Therefore, with the aim to evaluate the neurotoxic properties of Hcy on glial cells, we used a glioblastoma cell line as a study model. The viability of cells was assayed biochemically and cytologically. At a concentration around 50 μM in the culture medium D,L -Hcy induced cell death. It is noteworthy that Hcy induces cell death of human glial cells at concentrations encountered during mild hyperhomocysteinemia. Therefore, we propose that Hcy -induced impairment of neuronal functions along with damage of glial cells may contribute to the etiopathogenesis of neurodegenerative diseases associated with hyperhomocysteinemia., H. Škovierová, S. Mahmood, E. Blahovcová, J. Hatok, J. Lehotský, R. Murín., and Obsahuje bibliografii