The sequence of changes in circulating immune cells and in free radical production was studied during the small intestine reperfusion. Rat small intestine ischemia/reperfusion was induced by a 45 min superior mesenteric artery occlusion followed by a 4-hour reperfusion. Samples of peripheral blood were collected every 20 min during reperfusion. While the number of polymorphonuclear leukocytes increased significantly both in the sham-operated controls and the experimental group (about 400 % at the end of reperfusion), a decrease in lymphocyte counts to 60 % was observed in the experimental group only. Although there were no changes in the counts of total T lymphocytes, a significant reduction in B cell counts was observed. Flow-cytometrical measurements showed no changes in the Tc subpopulation, while the Th subpopulation increased in the experimental group only. Free radical generation in blood (luminometric measurements) increased gradually and reached an eight-fold level by the end of reperfusion in both groups. Thus, it has been shown that the increase in free radical production is mainly due to the increased number of polymorphonuclear leukocytes mobilized already at the initial stages of reperfusion. The reduction in B lymphocyte population is probably due to homing mechanisms., J. Hamar, I. Rácz, M. Číž, A. Lojek, É. Pállinger, J. Fűrész., and Obsahuje bibliografii
The purpose of this study was to compare markers of glycolytic metabolism in response to the Wingate test and the incremental test in road and mountain bike cyclists, who not different performance level and aerobic capacity. All cyclists executed the Wingate test and incremental test on a cycle ergometer. Maximal power and average power were determined during the Wingate test. During the incremental test the load was increased by 50 W every 3 min, until volitional exhaustion and maximal aerobic power (APmax), maximal oxygen uptake (VO2max), and time of VO2max plateau (Tplateau) were determined. Post-exercise measures of oxygen uptake (VO2post), carbon dioxide excretion, (VCO2post), and the ratio between VCO2/VO2 (RERpost) were collected for 3 min immediately after incremental test completion. Arterialized capillary blood was drawn to measure lactate (La-) and hydrogen (H+) ion concentrations in 3 min after each test. The data demonstrated significant differences between mountain bike and road cyclists for Tplateau, VO2post, VCO2post, La- which was higher-, and RERpost which was lower-, in mountain bike cyclists compare with road cyclists. No differences were observed between mountain bike and road cyclists for APmax, VO2max, H+ and parameters measured in the Wingate test. Increased time of VO2max plateau concomitant to larger post-exercise La- and VO2 values suggests greater anaerobic contribution during incremental testing efforts by mountain bike cyclists compared with road cyclists., P. Hebisz, R. Hebisz, J. Borkowski, M. Zatoń., and Obsahuje bibliografii
Leptin is produced by white adipose tissue and other cell types and is involved in both short- and long-term appetite control. Here we studied effects of star vation on serum, pituitary and hypothalamic levels of leptin during 72 h period. Each of the starved groups was sacrificed simultaneously with the group of ad libitum fed animals. The progression of the discrete starvation response phases was monitored by testing the blood glucose, free fatty acid, urea and corticosterone levels. Starvation caused biphasic increase in corticosterone and free fatty acid levels, and significant but transient decrease in urea and glucose levels. Starvation also abolished diurnal rhythm of changes in leptin concentrations in serum and hypothalamic and pituitary tissues. Only 6 h starving period was sufficient to lock serum leptin at low levels, whereas 12 h were needed to silence leptin production/secretion in hypothalamus for the whole examined period. In contrast, leptin production by pituitary tissues of starved animals required 24 h to reach minimum, followed by full recovery by the end of starvation period. These resu lts indicate the tissue specific pattern of leptin release and suggest that the locally produced leptin could activate its receptor in pituitary cells independently of serum levels of this hormone., P. Vujovic ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Vasoactive intestinal peptide (VIP) is a neuropeptide released from the autonomic nerves exerting multiple antiinflammatory effects. The aim of the present study was to investigate the impact of severe sepsis and hemofiltration in two settings on plasma and tissue concentrations of VIP in a porcine model of sepsis. Thirty-two pigs were di vided into 5 groups: 1) control group; 2) control group with conventional hemofiltration; 3) septic group; 4) septic group with conventional hemofiltration; 5) septic group with high-volume hemofiltration. Sepsis induced by faecal peritonitis continued for 22 hours. Hemofiltration was applied for the last 10 hours. Hemodynamic, inflammatory and oxidative stress parameters (heart rate, mean arterial pressure, cardiac output, systemic vascular resistance, plasma concentrations of tumor necrosis factor- α , interleukin-6, thiobarbituric acid reactive species, nitrate + nitrite, asymmetric dimethylarginine) and the systemic VIP concentrations were measured before faeces inoculation and at 12 and 22 hours of peritonitis. VIP tissue levels were determined in the left ventricle, mesenteric and coronary arteries. Sepsis induced significant increases in VIP concentrations in the plasma and mesenteric artery, but it decreased peptide levels in the coronary artery. Hemofiltration in both settings reduced concentrations of VIP in the mesenteric artery. In severe sepsis, VIP seems to be rapidly depleted from the coronary artery and, on the other hand, upregulated in the mesenteric artery. Hemofiltration in both settings has a tendency to drain away these upregulated tissue stores which could result in the limited secretory capacity of the peptide., J. Kuncová ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
a1_The tissue factor plays a crucial role in initiating blood coagulation after plaque rupture in patients with acute coronary syndrome. It is abundant in atherosclerotic plaques. Moreover, P-selectin, some cytokines, endotoxin and immune complexes can stimulate monocytes and induce the tissue factor expression on their surface. The aim of the study was to compare plasma levels of the tissue factor, tissue factor pathway inhibitor, P-selectin, E-selectin and ICAM-1 in patients with acute myocardial infarction, unstable angina pectoris, stable coronary artery disease and normal control subjects. In addition, plasma levels of the tissue factor, tissue factor pathway inhibitor, P-selectin, E-selectin and ICAM-1 were measured in the blood withdrawn from the coronary sinus in a subgroup of patients with unstable angina pectoris and stable coronary artery disease in which the difference between concentrations in the coronary sinus and systemic blood was calculated. A significant increase in tissue factor pathway inhibitor plasma levels was detected in patients with acute myocardial infarction (373.3±135.1 ng/ml, p<0.01) and unstable angina pectoris (119.6±86.9 ng/ml, p<0.05) in contrast to the patients with stable coronary artery disease (46.3±37.5 ng/ml) and normal subjects (45.1±14.3 ng/ml). The plasma levels of tissue factor pathway inhibitor were significantly increased both in the coronary sinus and systemic blood in the patients with unstable angina pectoris. There was only a non-significant trend to higher plasma levels of the tissue factor in patients with acute myocardial infarction and unstable angina pectoris as compared to the patients with stable coronary artery disease and normal subjects, the values being 129.1±30.2 pg/ml, 130.5±57.8 pg/ml, 120.2±45.1 pg/ml and 124.9±31.8 pg/ml, respectively., a2_Plasma levels of soluble P-selectin was only slightly, but non-significantly higher in patients with unstable angina pectoris and stable coronary artery disease (184.2±85.4 ng/ml and 201.6±67.9 ng/ml, respectively) than in patients with the acute myocardial infarction (157.4±88.4 ng/ml) or normal subjects (151.4±47.1 ng/ml). The difference in plasma levels of soluble ICAM-1 between the blood withdrawn from the coronary sinus and systemic circulation correlated significantly with the corresponding difference in plasma levels of soluble P-selectin and E-selectin. In conclusion, the tissue factor and the tissue factor pathway inhibitor play a crucial role in the initiation of arterial thrombosis. The tissue factor pathway inhibitor levels are increased both in the systemic blood and in the coronary sinus of patients with the acute coronary syndrome., M. Malý, J. Vojáček, V. Hraboš, M. Semrád, M. Mates, J. Kvasnička, P. Salaj, V. Durdil., and Obsahuje bibliografii
Smoking is the most important cardiovascular (CV) risk factor. Stopping smoking halves the CV risk. Every clinician should provide a brief intervention with smokers. Intensive treatment should be available to those who need it. There are 37 Centers for Tobacco Dependence in the Czech Republic, which offer treatment including a psychobehavioral intervention and pharmacotherapy (varenicline, nicotine, bupropion). Czech physicians, pharmacists and nurses are regularly educated about smoking cessation. We describe the results of intensive treatment offered by our centers. Treatment includes screening (1 h), an intervention (2 h), and follow-up visits during the next 12 months. Among 3532 patients, 34.3 % had CO-validated abstinence at 12-months (including 489 patients who attended the screening visit + only the 12-month follow up visit). Among patients who underwent the intervention, the abstinence rate was 38.2 %. The majority of patients who underwent the intervention (N=2470) used some form of pharmacotherapy. After one year, the abstinence rate was 43.4 %, compared to 15.9 % (N=573) without pharmacotherapy. Only 28 % of patients came on the recommendation of a physician. Despite the decrease in CV risk following smoking cessation and the effectiveness of treatment, centers are underutilized., E. Králíková, A. Kmeťová, L. Štěpánková, K. Zvolská, V. Felbrová, S. Kulovaná, Z. Bortlíček, M. Blaha, K. Fraser., and Obsahuje bibliografii
Hypertrophied hearts are known for increased risk of arrhythmias and are linked with reduced ischemic tolerance. However, still little is known about state characterized only by increased left ventricle (LV) mass fraction. Seventeen isolated rabbit hearts with various LV mass were divided into two groups according to LV weight/heart weight ratio (LVW/HW ratio), namely group H and L (with higher and lower LVW/HW ratio, respectively) and underwent three short cycles of global ischemia and reperfusion. The differences in electrogram (heart rate, QRSmax, mean number, onset and dominant form of ventricular premature beats) and in biochemical markers of myocardial injury (creatine kinase, lactate dehydrogenase - LDH) and lipid peroxidation (4-hydroxy-2-nonenal - 4-HNE) were studied. As compared to group L, hearts in group H exhibited lower tolerance to ischemia expressed as higher incidence and severity of arrhythmias in the first ischemic period as well as increase of LDH and 4-HNE after the first reperfusion. In the third cycle of ischemia-reperfusion, the preconditioning effect was observed in both electrophysiological parameters and LDH release in group H. Our results showed consistent trends when comparing changes in electrograms and biochemical markers. Moreover, 4-HNE seems to be good potential parameter of moderate membrane alteration following ischemia-reperfusion injury., M. Hlaváčová, V. Olejníčková, M. Ronzhina, T. Stračina, O. Janoušek, M. Nováková, P. Babula, J. Kolářová, I. Provazník, H. Paulová., and Obsahuje bibliografii
Clinical and experimental studies have repeatedly indicated that overloaded hearts have a higher vulnerability to ischemia/reperfusion injury. The aim of the present study was to answer the question whether the degree of tolerance to oxygen deprivation in hearts of spontaneously hypertensive rats (SHR) may be sex-dependent. For this purpose, adult SHR and their normotensive control Wistar Kyoto (WKY) rats were used. The isolated hearts were perfused according to Langendorff at constant pressure (proportionally adjusted to the blood pressure in vivo). Recovery of contractile parameters (left ventricular systolic, diastolic and developed pressure as well as the peak rate of developed pressure) was measured during reperfusion after 20 min of global no-flow ischemia in 5 min intervals. Mean arterial blood pressure was measured by direct puncture of carotid artery under light ether anesthesia in a separate group of animals. The degree of hypertension was comparable in both sexes of SHR. The recovery of contractile functions in SHR males and females was significantly lower than in WKY rats during the whole investigated period. There was no sex difference in the recovery of WKY animals; on the other hand, the recovery was significantly better in SHR females than in SHR males. It may be concluded that the hearts of female SHR are more resistant to ischemia/reperfusion injury as compared with male SHR. This fact could have important clinical implications for the treatment of cardiovascular disease in women., J. Bešík, O. Szárszoi, J. Kuneš, I. Netuka, J. Malý, F. Kolář, J. Pirk, B. Ošťádal., and Obsahuje bibliografii a bibliografické odkazy
The objective of our study was to assess the influence of mechanical ventilation on healthy body organs. Fifteen piglets (aged 6 weeks, 19-27 kg) were anesthetized, instrumented, and divided into three groups: Group A - spontaneously breathing, group B - mechanically ventilated with tidal volume 6 ml/kg, and group C - ventilated with tidal volume 10 ml/kg for 12 hours. The parameters of lung, heart, liver and kidney functions neurohumoral regulation and systemic inflammatory reaction were recorded initially (time-1) and after 12 hours (time-12) of mechanical ventilation. At the onset of experiment (time-1) the levels of soluble adhesive molecules were higher (CAM; P<0.01), glomerular filtration index and free water clearance were lower (P<0.05) in both ventilated groups than in group A. Right ventricle myocardial performance index was higher (RIMP; P<0.05) in group C when compared with group A. Levels of CAM (P<0.05) and creatinine clearance (P<0.01) were higher, free water clearance was lower (P<0.05) in group C when compared to group B. At time-12 the RIMP (P<0.05) and levels of CAM were increased (P<0.01), creatinine clearance was decreased (P<0.05) in both ventilated groups compared to the same parameter at time-1. Ventilation index was higher (P<0.05), and hypoxemic index was lower (P<0.01) in group C when compared to group B. In conclusion, this study showed that mechanical ventilation induced changes compatible with early inflammatory response in healthy animals. Higher tidal volumes had detrimental effect on ventilatory parameters, reduced myocardial performance and potentiated adverse reaction of other organs., J. Kobr ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
The present study investigated cardiac function in hearts of mice with total deficiency of the β1-, β2- and β3-adrenoceptors (TKO) in comparison to wildtype mice (WT). We investigated cardiac morphology and echocardiographic function, measured protein expression of Ca2+-regulatory proteins, SERCA 2a activity, myofibrillar function, and performed running wheel tests. Heart weight and heart-to-body weight ratio were significantly smaller in TKO as compared to WT. This was accompanied by a decrease in the size of the cardiomyocytes in TKO. Heart rate and ejection fraction were significantly diminished in TKO as compared to WT. Protein expressions of SERCA 2a, ryanodine receptor and Na+/Ca2+-exchanger were similar in TKO and WT mice, but phospholamban protein expression was increased. PKAdependent phosphorylation of phospholamban at serine 16 was absent and CaMKII-dependent phosphorylation at threonine 17 was decreased in TKO. All alterations were paralleled by a decrease in SERCA 2a-activity. A similar maximal calciumdependent tension but an increased myofibrillar calciumsensitivity was measured in TKO as compared to WT. We did not observe relevant functional impairments of TKO in running wheel tests. In the absence of β-agonistic stimulation, SERCA 2a activity is mainly regulated by alterations of phospholamban expression and phosphorylation. The decreased SERCA 2a activity following β-adrenoceptor deficiency may be partly compensated by an increased myofibrillar calcium-sensitivity., S. Lee ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy