Chronic kidney disease (CKD) is associated with increased concentration of intracellular calcium, which is pathological and may lead to irreversible damage of cell functions and structures. The aim of our study was to investigate the impact of 6 months vitamin D3 supplementation (14 000 IU/week) on free cytosolic calcium concentration ([Ca2+]i) and on the plasma membrane calcium ATPase (PMCA) activity of patients with CKD stage 2-3. PMCA activity of patients was also compared to that of healthy volunteers. Vitamin D3 supplementation of CKD patients resulted in the decrease of [Ca2+]i (119.79±5.87 nmol/l vs. 105.36± 3.59 nmol/l, n=14, P<0.001), whereas PMCA activity of CKD patients (38.75±22.89 nmol Pi/mg/h) remained unchanged after vitamin D3 supplementation (40.96±17.74 nmol Pi/mg/h, n=14). PMCA activity of early stage CKD patients before supplementation of vitamin D3, was reduced by 34 % (42.01±20.64 nmol Pi/mg/h) in comparison to healthy volunteers (63.68±20.32 nmol Pi/mg/h, n=28, P<0.001). These results indicate that vitamin D3 supplementation had a lowering effect on [Ca2+]i and negligible effect on PMCA activity in CKD patients., M. Morvová Jr., I. Lajdová, V. Spustová, M. Zvarík, L. Šikurová., and Obsahuje bibliografii
Neuroprotective effects of estrogens and progesterone have been widely studied in various experimental models. The present study was designed to compare possible neuroprotective effects of 17alpha-estradiol, 17beta-estradiol, and progesterone on oxidative stress in rats subjecte d to global cerebral ischemia. Global cerebral ischemia was induced in ovariectomized female rats by four vessel occlusion for 10 min. Following 72 h of reperfusion, levels of malondialdehyde (MDA, oxidative stress marker), and reduced glutathione (GSH, major endogenous antioxidant) were assessed in hippocampus, striatum and cortex of rats treated with either 17alpha-estradiol, 17beta-estradiol, progesterone or estradiol + progesterone beforehand. Steroid administration ameliorated ischemia-induced decrease in GSH and increase in MDA levels. Our data offers additional evidence that estrogens and progesterone or combination of two exert a remarkable neuroprotective effect reducing oxidative stress., V. H. Ozacmak, H. Sayan., and Obsahuje seznam literatury
In cardiac surgical patients we investigated the effects of cardiopulmonary bypass (CPB) with a hollow fiber membrane oxygenator on blood clotting measured by thromboelastography (TEG). We found only a minimal change in the strength of blood clot described either by the TEG parameter MA (maximum amplitude) or by the shear modulus G calculated from MA. After CPB there was also a significant tendency towards hypercoagulation as defined by shortened parameters R, K and increased ?-angle. After comparison with published data obtained in cardiac surgical patients using a bubble oxygenator we conclude that currently used extracorporeal technology exerts a less negative influence on blood clotting than had been conceived previously., M. Horáček, K. Cvachovec., and Obsahuje bibliografii
Obesity is increasing at an alarming rate globally. Several studies have shown that premenopausal women have a reduced risk of CV disease and a reduced myocardial susceptibility to ischemia/reperfusion injury. The effect of obesity on myocardial tolerance to ischemia in women has not been established. To determine how obesity affects myocardial susceptibility to ischemia/reperfusion injury in both males and females, we fed male and female Wistar rats a high caloric diet (HCD) or a control rat chow diet (CD) for 18 weeks. Rats were subsequently fasted overnight, anesthetized and blood was collected. In separate experiments, 18-week-fed (HCD and CD) rats underwent 45 min in vivo coronary artery ligation (CAL) followed by 2 hours reperfusion. Hearts were stained with TTC and infarct size determined. Both male and female HCD fed rats had increased body and visceral fat weights. Homeostasis model assessment (HOMA) index values were 13.95±3.04 for CD and 33.58±9.39 for HCD male rats (p<0.01) and 2.98±0.64 for CD and 2.99±0.72 for HCD fed female rats. Male HCD fed rats had larger infarct sizes than CD fed littermates (43.2±9.3 % vs. 24.4±7.6 %, p<0.05). Female HCD and CD diet fed rats had comparable infarct sizes (31.8±4.3 % vs. 23.9±3.3 %). We conclude that male rats on the HCD became viscerally obese, dyslipidemic and insulin-resistant, while female HCD fed rats became viscerally obese without developing dyslipidemia or insulin resistance. Obesity increased myocardial infarct size in males but not the females., C. Clark ... [et al.]., and Obsahuje seznam literatury
The present study investigated the effects of head cooling during endurance cycling on performance and the serotonergic neuroendocrine response to exercise in the heat. Subjects exercised at 75 % VO2max to volitional fatigue on a cycle ergometer at an ambient temperature of 29±1.0 °C, with a relative humidity of approximately 50 %. Head cooling resulted in a 51 % (p<0.01) improvement in exercise time to fatigue and Borg Scale ratings of perceived exertion were significantly lower throughout the exercise period with cooling (p<0.01). There were no indications of peripheral mechanisms of fatigue either with, or without, head cooling, indicating the importance of central mechanisms. Exercise in the heat caused the release of prolactin in response to the rise in rectal temperature. Head cooling largely abolished the prolactin response while having no effect on rectal temperature. Tympanic temperature and sinus skin temperature were reduced by head cooling and remained low throughout the exercise. It is suggested that there is a co-ordinated response to exercise involving thermoregulation, neuroendocrine secretion and behavioural adaptations that may originate in the hypothalamus or associated areas of the brain. Our results are consistent with the effects of head cooling being mediated by both direct cooling of the brain and modified cerebral artery blood flow, but an action of peripheral thermoreceptors cannot be excluded., L. Ansley, G. Marvin, A. Sharma, M. J. Kendall, D. A. Jones, M. W. Bridge., and Obsahuje bibliografii a bibliografické odkazy
Cytochrome oxidase activity from the retina can be enhanced or depressed by free radical-mediated reactions both in positive and negative aspect. The greatest effect was exerted by ischemia/reperfusion, which significantly increased the fluorescent products of lipid peroxidation (358 %, P<0.01) and inhibited the enzyme activity (14 %, P<0.001). After hyperoxia the fluorescent products slightly increased (192 %, P< 0.05) as well as the enzyme activity (133 %, P<0.05). Hypoxia had no effect on any of these parameters. Specific changes in the composition of fluorophores after ischemia/reperfusion were revealed in the fluorescence spectra. The fact that increased lipid peroxidation after hyperoxia and after ischemia/reperfusion does not produce the same effect upon cytochrome oxidase activity might be explained by changes in the kinetic behavior of cytochrome oxidase. In the control enzyme preparation, two binding sites for cytochrome c were observed. One was of the low-affinity (Km=60 mM) and the other of the high-affinity (Km=1.12 mM). After in vitro-initiated lipid peroxidation, the low-affinity binding site was lost and the activity measured under "optimum" conditions at a single cytochrome concentration was higher than in the controls. This implies that oxidative damage to cytochrome oxidase in vivo can be site-specific and its extent should be estimated by performing detailed kinetic analysis as otherwise the results might be misleading., A. Šišková, J. Wilhelm., and Obsahuje bibliografii
Bupivacaine is a widely used long-acting local anaesthetic. In clinical practice, a mixture of bupivacaine and lidocaine is often used in order to combine the faster onset of sensory blockade of lidocaine with more profound and longer duration of blockade by bupivacaine. The aim of this study was to compare the cardiotoxicity of large doses of bupivacaine and mixture of bupivacaine with lidocaine in the isolated rat heart and to estimate whether or not the addition of lidocaine in clinically relevant concentration increases bupivacaine-induced toxicity. Experiments were performed on 21 adult male rats divided into three groups: B (6 μg/ml bupivacaine), BL (6 μg/ml bupivacaine and 12 μg/ml lidocaine) and L (12 μg/ml lidocaine). The experiment consisted of three 30 min periods: stabilisation, perfusion and washout. The isolated hearts were perfused according to Langendorff with Krebs-Henseleit solution at constant pressure (80 mmHg) and 37 °C (CaCl2 1.25 mM) and the heart rate (based on RR interval assessment), PQ and QRS intervals were measured. The present study shows that the mixture of tested anaesthetics - bupivacaine and lidocaine - impairs the intraventricular conduction parameters (QRS interval prolongation) to a lesser extent than bupivacaine itself, and that this effect is marked mainly at the beginning of perfusion., I. Křikava ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteen-week-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 μg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTX-sensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension., S. Čačányiová, F. Kristek, J. Kuneš, J. Zicha., and Obsahuje bibliografii a bibliografické odkazy
A higher mean arterial pressure (MAP) achieved by norepinephrine up-titration may improve organ blood flow in critically ill, whereas norepinephrine-induced afterload rise might worsen myocardial function. Our aim was to assess the effects of norepinephrine dose titration on global hemodynamics in cardiogenic shock. We prospectively evaluated 12 mechanically ventilated euvolemic patients (aged 67±12 years) in cardiogenic shock (10 patients acute myocardial infarction, 1 patient dilated cardiomyopathy, 1 patient decompensated aortic stenosis). Hemodynamic monitoring included arterial and Swan-Ganz catheters. The first data were obtained at MAP of 65 mm Hg, then the norepinephrine dose was increased over 40 min to achieve MAP of 85 mm Hg. Finally, the norepinephrine-dose was tapered over 40 min to achieve MAP of 65 mm Hg. Norepinephrine up-titration increased MAP to the predefined values in all patients with concomitant mild increase in filling pressures and heart rate. Systemic vascular resistance increased, whereas cardiac output remained unchanged. During norepinephrine down-titration, all hemodynamic parameters returned to baseline values. We observed no changes in lactate levels and mixed venous oxygen saturation. Our data suggest that short-term norepinephrine dose up-titration in cardiogenic shock patients treated or pretreated with inotropes was tolerated well by the diseased heart., R. Rokyta, Jr ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy