Browsing by Author "Zivkovic, V. (55352337400)"

Despite worldwide popularity of soccer, there are still insufficient data about the effects of training process on oxidative stress-induced damage, which may occur during chronic exercise. The present study aimed to determine the effects of a six-month training programme on basal redox status of young male soccer players. The study included 26 male soccer players, aged 12-13, who participated in a six-month training programme, and 26 agematched non-athletes who were not implemented in the training process. Blood samples were collected (before and after six-month training programme) in order to measure the following oxidative stress markers: index of lipid peroxidation (measured as TBARS), nitrites (NO2-), superoxide anion radical (O 2-), hydrogen peroxide (H2O2), superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) level. After six months, the levels of TBARS and NO2- were significantly increased, while the O2- and H 2O2 remained unchanged. On the other hand, SOD and CAT activity increased, while GSH decreased. A carefully prepared training programme could strengthen most components of antioxidant defence systems and, except lipid peroxidation, does not promote oxidative stress in response to regular physical activity. These findings could help in the improvement of training programmes for young athletes. © 2013 Akadémiai Kiadó, Budapest.

In patients with unreconstructable arterial occlusive disease distal venous arterialization (DVA) seems to be a promising option in the treatment. The goals of this prospective study were to assess clinical efficiency and possible impact of DVA on tissue damage by estimating oxidative status of patients with critical limb ischemia treated with this procedure. The subjects were 60 randomized patients: 30 were undergoing DVA and 30 were treated with antiaggregation therapy. During the mean follow-up period (6.13 ± 4.32 months for DVA vs. 6.74 ± 0.5 months for antiaggregation therapy) survival (p < 0.01), limb salvage (p < 0.001), pain relief (p < 0.001) and wound healing (p < 0.001) rates were significantly different between the two groups of patients in favor of the DVA group. Ten minutes after declamping we observed a decreasing trend in the lactate level in the blood of the deep venous system (p < 0.001). Also, on postoperative day 7 digital systolic pressure and digital-brachial index were higher than before the operation (p < 0.001). In blood samples collected immediately before and successively at 1, 3, 5 and 10 min postoperatively, prooxidative status (thiobarbituric acid reactive substances, O2-, H2O2 and nitric oxide) and antioxidative enzymes (superoxide dismutase, catalase and glutathione reductase) were determined spectrophotometrically. Using the nonparametric Friedman test, we noted statistically nonsignificant differences (p > 0.05) in values of both prooxidative parameters and enzymes of the antioxidative defense system, before and successively at 1, 3, 5 and 10 min after operation. These results indicate that there was no statistically significant reperfusion injury after revascularization, which could have been expected after this surgical procedure, thus confirming its validity in these patients. Copyright © 2012 S. Karger AG, Basel.

It has been assumed that the cardioprotective effects of propofol are due to its non-anesthetic pleiotropic cardiac and vasodilator effects, in which gasotransmitters (NO, H2S, and CO) as well as calcium influx could be involved. The study on isolated rat heart was performed using 4 experimental groups (n = 7 in each): (1) bolus injection of propofol (100 mg/kg body mass, i.p.); (2) L-NAME (NO synthase inhibitor, 60 mg/kg body mass, i.p.) + propofol; (3) DL-PAG (H2S synthase inhibitor, 50 mg/kg body mass, i.p.) + propofol; (4) ZnPPIX (CO synthase inhibitor, 50 μmol/kg body mass, i.p.) + propofol. Before and after the verapamil (3 μmol/L) administration, cardiodynamic parameters were recorded (dp/dtmax, dp/dtmin, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate, coronary flow), as well as coronary and cardiac oxidative stress parameters. The results showed significant increases of diastolic left ventricular pressure following NO and CO inhibition, but also increases of coronary flow following H2S and CO inhibition. Following verapamil administration, significant decreases of dp/dtmax were noted after NO and CO inhibition, then increase of diastolic left ventricular pressure following CO inhibition, and increase of coronary flow following NO, H2S, or CO inhibition. Oxidative stress markers were increased but catalase activity was significantly decreased in cardiac tissue. Gasotransmitters and calcium influx are involved in pleiotropic cardiovascular effects of propofol in male Wistar rats. © 2019, Canadian Science Publishing. All rights reserved.

It has been assumed that the cardioprotective effects of propofol are due to its non-anesthetic pleiotropic cardiac and vasodilator effects, in which gasotransmitters (NO, H2S, and CO) as well as calcium influx could be involved. The study on isolated rat heart was performed using 4 experimental groups (n = 7 in each): (1) bolus injection of propofol (100 mg/kg body mass, i.p.); (2) L-NAME (NO synthase inhibitor, 60 mg/kg body mass, i.p.) + propofol; (3) DL-PAG (H2S synthase inhibitor, 50 mg/kg body mass, i.p.) + propofol; (4) ZnPPIX (CO synthase inhibitor, 50 μmol/kg body mass, i.p.) + propofol. Before and after the verapamil (3 μmol/L) administration, cardiodynamic parameters were recorded (dp/dtmax, dp/dtmin, systolic left ventricular pressure, diastolic left ventricular pressure, heart rate, coronary flow), as well as coronary and cardiac oxidative stress parameters. The results showed significant increases of diastolic left ventricular pressure following NO and CO inhibition, but also increases of coronary flow following H2S and CO inhibition. Following verapamil administration, significant decreases of dp/dtmax were noted after NO and CO inhibition, then increase of diastolic left ventricular pressure following CO inhibition, and increase of coronary flow following NO, H2S, or CO inhibition. Oxidative stress markers were increased but catalase activity was significantly decreased in cardiac tissue. Gasotransmitters and calcium influx are involved in pleiotropic cardiovascular effects of propofol in male Wistar rats. © 2019, Canadian Science Publishing. All rights reserved.

This study aimed to investigate the effects of propofol through evaluating its interaction with nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO). Wistar male rats were divided in 4 groups: (1) bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (2) (formula presented)-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor, 60 mg/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (3) DL-propargylglycine (DL-PAG; H2S synthase inhibitor, 50 mg/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (4) zinc protoporphyrin IX (ZnPPIX; CO synthase inhibitor, 50 μmol/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.). Increased levels of albumins, low-density lipoproteins, alkaline phosphatase, amylase, high-sensitivity Troponin T, and fibrinogen were found in L-NAME + propofol group. Platelet crit, platelet count, total cholesterol, and high-density lipoproteins were elevated in ZnPPIX + propofol group. Hydrogen peroxide was increased in all groups treated with gasotransmitters inhibitors. Reduced glutathione was reduced in all groups, superoxide dismutase activity only in L-NAME + propofol. The effect of propofol on various biochemical, haematological, and oxidative stress markers may be at least in part mediated through interaction with 3 estimated gasotransmitters. © 2019, Canadian Science Publishing. All rights reserved.

This study aimed to investigate the effects of propofol through evaluating its interaction with nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO). Wistar male rats were divided in 4 groups: (1) bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (2) (formula presented)-nitro-L-arginine methyl ester (L-NAME; NO synthase inhibitor, 60 mg/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (3) DL-propargylglycine (DL-PAG; H2S synthase inhibitor, 50 mg/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (4) zinc protoporphyrin IX (ZnPPIX; CO synthase inhibitor, 50 μmol/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.). Increased levels of albumins, low-density lipoproteins, alkaline phosphatase, amylase, high-sensitivity Troponin T, and fibrinogen were found in L-NAME + propofol group. Platelet crit, platelet count, total cholesterol, and high-density lipoproteins were elevated in ZnPPIX + propofol group. Hydrogen peroxide was increased in all groups treated with gasotransmitters inhibitors. Reduced glutathione was reduced in all groups, superoxide dismutase activity only in L-NAME + propofol. The effect of propofol on various biochemical, haematological, and oxidative stress markers may be at least in part mediated through interaction with 3 estimated gasotransmitters. © 2019, Canadian Science Publishing. All rights reserved.

This study aimed to assess the role of H2S in homocysteine-induced cardiodynamic effects in the isolated rat heart. The hearts were retrogradely perfused according to the Langendorff technique. The maximum and minimum rates of pressure in the left ventricle (dp/dt max, dp/dt min), systolic and diastolic left ventricular pressures (SLVP, DLVP), heart rate (HR), and coronary flow (CF) were measured. A spectrophotometrical method was used to measure the following oxidative stress markers: index of lipid peroxidation (thiobarbituric acid reactive substances, TBARS), nitrite level (NO2-), superoxide anion radicals (O2•-), and hydrogen peroxide (H2O2) concentrations. The administration of 10 μmol/l DL-homocysteine (DL-Hcy) alone decreased dp/dt max, SLVP, and CF but did not change any oxidative stress parameters. The administration of 10 μmol/l DL-propargylglycine (DL-PAG) decreased all cardiodynamic parameters and increased the concentration of O2•-. The co-administration of DL-Hcy and DL-PAG induced a significant decrease in all estimated cardiodynamic parameters and decreased the concentration of NO2- and O2 •- but increased the levels of TBARS and H2O2. Homocysteine shows a lower pro-oxidative effect in the presence of hydrogen sulfide (H2S), which indicates a potential anti-oxidative capacity of H2S. © 2016 Akadémiai Kiadó, Budapest.