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Tramadol in pediatric patients undergoing UGIE provided sedation as efficient as fentanyl with a better hemodynamic and respiratory stability and provided a superior safety and tolerance in younger children.

Objectives. Following ischemia/reperfusion injury, antioxidant defense mechanisms may remain insufficient depending on the duration of ischemia which is caused by any reason (MI, after percutaneous coronary intervention, during cardiac surgery). After that, free oxygen radicals increasing within the cell cause structural deterioration. Cytokines which activate a series of reactions that cause tissue damage and inflammatory response are released during reperfusion of ischemic tissues. In this study, we aimed to compare the effects of dexmedetomidine and ketamine in cardiac ischemia/reperfusion injury. Material and Methods. The study included 18 rats randomly divided into three groups. Group I/R (n = 6): control, Group I/R-K (n = 6): ketamine, and Group I/R-D (n = 6): dexmedetomidine. Before the 10 min surgery, after the 20 min ischemia and 20 min reperfusion period, hemodynamic parameters were compared among the three groups. After the 45 min ischemia and 120 min reperfusion period, tissue samples were obtained from the rat hearts, and MDA, SOD, GSH-Px, IL-1β and TNF-α levels were compared. Results. MDA and GSH-Px levels were significantly higher in the control group compared to the ketamine and dexmedetomidine groups. However, both levels were similar in the ketamine and dexmedetomidine groups. SOD levels were significantly lower in the ketamine and dexmedetomidine groups compared to the control group, but they were similar in the ketamine and dexmedetomidine groups. IL-1β levels were similar in all groups. TNF-α levels were significantly lower in the ketamine and dexmedetomidine groups compared to the control group. They were similar in the ketamine and dexmedetomidine groups. Conclusions. According to our study, it can be concluded that dexmedetomidine and ketamine have similar effects on reducing myocardial ischemia reperfusion injury. Dexmedetomidine provides better heart rate control but causes hypotension, so, because of cardiac depression, we think that its clinical use may necessitate further investigation (Adv Clin Exp Med 2014, 23, 5, 683-689).Key words: dexmedetomidine, ketamine, cardiac ischemia/reperfusion injury. Coronary artery disease (CAD) is one of the most common causes of morbidity and mortality at the present time and is also responsible for about half of the deaths in developed countries. CAD is the result of the accumulation of atheromatous plaques within the walls of the coronary arteries. The deposition of the plaque in the lumen of an artery causes a narrowing of the lumen of the artery by decreasing its diameter. Atherosclerotic plaques reduce the blood flow due to narrowing of the lumen and coronary artery vasospasm.Ischemia/reperfusion (I/R) injury constitutes the basis of the pathophysiology due to angina pectoris, myocardial infarction (MI), cerebral

Background:The aim of this study was to assess the early postoperative pulmonary function and arterial blood gases in patients who have undergone open versus laparoscopic nephrectomy.Materials and Methods:Forty patients were randomly assigned to undergo laparoscopic (LN, n=20) or open nephrectomy (ON, n=20). Pulmonary function tests including forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), forced expiratory volume at 25% (FEF25), forced expiratory volume at 50% (FEF50), forced expiratory volume at 25% to 75% (FEF25–75), forced expiratory volume in 1 second (FIV1) and peak expiratory flow (PEF) were performed one day before the operation and on the postoperative day 1. The arterial blood gas analysis (pH, pCO2, pO2, SaO2) was made at breathing room preoperatively, in the recovery phase and on postoperative day 1.Results:All spirometric variables decreased after both open and laparoscopic nephrectomy on postoperative day 1. FEV1, FVC, FEF25 and FEF25–75 values decreased on postoperative day 1 (39.7%, 37.4%, 27.7%, 51.8% respectively) in the open surgery group and they were significantly lower in laparoscopic group (29.9%, 32.5%, 23.2%, 44.5% respectively). There were no significant differences in FEF50, PEF and FIV1 between the groups. The SaO2 and pO2 values also decreased in both groups. During early recovery, pH decreased while pCO2 increased significantly but they returned to preoperative values on postoperative day 1 in both groups.Conclusion:Laparoscopic nephrectomy is better than open nephrectomy considering pulmonary functions.

BACKGROUND: Several animal studies showed benefi cial effects of thoracic epidural anesthesia (TEA) in hippocampal, mesenteric and myocardial IR injury (2-4). In this study, we investigated the effects of epidural bupivacaine on hepatic ischemia reperfusion injury in a rat model. MATERIAL AND METHODS: Eighteen rats were randomly divided into three groups each containing 6 animals. The rats in Group C had sham laparotomy. The rats in the Group S were subjected to liver IR through laparotomy and 20 mcg/kg/h 0.9 % NaCl was administered to these rats via an epidural catheter. The rats in the Group B were subjected to liver IR and were given 20 mcg/kg/h bupivacaine via an epidural catheter. Liver tissue was harvested for MDA analysis, apoptosis and histopathological examination after 60 minutes of ischemia followed by 360 minutes of reperfusion. Blood samples were also collected for TNF-α, IL-1β, AST and ALT analysis. RESULTS: The AST and ALT levels were higher in ischemia and reperfusion group, which received only normal saline via the thoracic epidural catheter, compared to the sham group. In the ischemia reperfusion group, which received bupivacaine via the epidural catheter, IL-1 levels were signifi cantly higher than in the other groups. TNF-α levels were higher in the Groups S and B compared to the sham group. Bupivacaine administration induced apoptosis in all animals. CONCLUSION: These results showed that thoracic epidural bupivacaine was not a suitable agent for preventing infl ammatory response and lipid peroxidation in experimental hepatic IR injury in rats. Moreover, epidural bupivacaine triggered apoptosis in hepatocytes. Further research is needed as there are no studies in literature investigate the effects of epidural bupivacaine on hepatic ischemia reperfusion injury (Tab. 3, Fig. 3, Ref. 34). Text in PDF www.elis.sk.