Nurdan Bedirli

Hepatic Energy Metabolism and the Differential Protective Effects of Sevoflurane and Isoflurane Anesthesia in a Rat Hepatic Ischemia-Reperfusion Injury Model

BACKGROUND: We investigated the effects of isoflurane and sevoflurane in a warm liver ischemia-reperfusion (IR) model on cytokines, hepatic tissue blood flow (HTBF), energy content, and liver structure. METHODS: Seventy-two Wistar rats were randomly assigned into 1 of 3 groups: Control group, no volatile anesthetics; sevoflurane group, 2% sevoflurane; isoflurane group, 1.5% isoflurane. Thirty minutes after the start of volatile anesthetics, rats were subjected to 45 min hepatic ischemia and 2 and 4 h of reperfusion. Rats were killed at the end of ischemia, 2 and 4 h of reperfusion. Aspartate aminotransferase and alanine aminotransferase, HTBF, malondialdehyde, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, energy charge, and histologic examination were used to evaluate the extent of liver injury. RESULTS: Serum alanine aminotransferase and aspartate aminotransferase levels were similar in control and isoflurane groups while there was a significant decrease in the sevoflurane group in the postischemic period (P < 0.01). HTBF was remarkably better in the sevoflurane group than in the isoflurane group and worse in the control group. Tissue malondialdehyde levels were significantly low in the sevoflurane group compared with the isoflurane group at 2 h of reperfusion (P < 0.05) and reached its maximum value in the postischemic period in the control group. After ischemia, 2 and 4 h of reperfusion, tumor necrosis factor-α and interleukin-1β values were lowest in the sevoflurane group and highest in the control group but it was not statistically significant (P > 0.05). In the sevoflurane group, hepatic adenosine triphosphate and energy charge were significantly high at all measurement times. At the postischemic period, energy charge was lower compared with the sevoflurane and isoflurane groups. The degree of hepatocyte injury was small in the sevoflurane group. CONCLUSIONS: Clinically relevant concentrations of sevoflurane given before, during, and after hepatic ischemia protected the liver against IR injury, whereas the effects of isoflurane on hepatic IR injury were not notable.

Sevoflurane and isoflurane preconditioning provides neuroprotection by inhibition of apoptosis-related mRNA expression in a rat model of focal cerebral ischemia.

Background: This study aimed to examine the effects of sevoflurane or isoflurane preconditioning on cerebral ischemia/reperfusion–induced inflammation, oxidative stress, and lipid peroxidation and test the hypothesis that the underlining mechanism of the protective effect of preconditioning involves changes in the apoptotic gene expression profiles in an experimental model of middle cerebral artery occlusion in rats. Methods: Twenty-four adult male rats were randomly divided into 3 groups: control (n=8), sevoflurane (n=8), and isoflurane (n=8). For preconditioning, these 3 groups were exposed to 40% O2, 2% sevoflurane, and 1.5% isoflurane, respectively, for 60 minutes, followed immediately by 1 hour of middle cerebral artery occlusion and then 6 hours of reperfusion. Blood and brain tissue samples were collected for determination of blood gas tension, tumor necrosis factor-&agr;, interleukin-6, and interleukin-1&bgr;. Brain tissue samples were collected for determination of the wet/dry ratio, myeloperoxidase, malondialdehyde, and total RNA and also for histologic examinations. Results: Tumor necrosis factor-&agr;, interleukin-1&bgr;, and myeloperoxidase levels decreased and antioxidant enzyme levels increased in the sevoflurane group compared with the control and isoflurane groups. Proapoptotic genes (Tnf, Tnfrsf10b, and Tp53) downregulated and antiapoptotic genes (Aven, Bcl2, Bcl2l2, and Prok2) upregulated with sevoflurane treatment compared with the isoflurane and control groups. Both isoflurane and sevoflurane pretreatment decreased malondialdehyde, Dffb, the wet/dry ratio, and injury score and upregulated Bax and Apaf 1 compared with the control group. Conclusions: Sevoflurane and isoflurane preconditioning ameliorates inflammation, cerebral lipid peroxidation, and histologic injury. Downregulation of proapoptotic molecules and upregulation of antiapoptotic molecules may be associated with this effect.

Volatile anesthetic preconditioning attenuated sepsis induced lung inflammation

BACKGROUND This study aimed to evaluate the differential protective effects of isoflurane or sevoflurane on lung inflammation in a rat model of cecal ligation and puncture (CLP) induced sepsis. METHODS Seventy-two rats were assigned to control, sevoflurane, or isoflurane groups. At 2 and 4 h, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β), nitrate/nitrate levels (NO), total antioxidant capacity (TAC), and intercellular cell adhesion molecule-1 (ICAM-1) were determined. At 12 and 24 h, malondialdehyde (MDA), myeloperoxidase (MPO), and histologic changes were evaluated. Survival was monitored for 7 d after CLP. RESULTS Sevoflurane (75%) and isoflurane (63%) significantly improved survival rate compared with control rats (38%). When sevoflurane and isoflurane groups were compared, sevoflurane pretreatment showed significant decrease in NO at 2 h [1045 (803-1274)/1570 (1174-2239) and 4 h [817 (499-1171)/1493 (794-2080)]; increase in TAC at 4 h [580.0 (387-751)/320 (239-512)]; decrease in MDA at 12 h [2.5 (1.1-4.2)/5.4 (4-73)] and 24 h [10.8 (6.0-14.0)/15.9 (9-28)]; and decrease in MPO at 24 h [145.8 (81-260)/232 (148-346)]. The difference in the ICAM-1 expression of the isoflurane and sevoflurane groups was not significant at both measurement times. The architectural integrity of the alveoli was preserved in all the groups. The injury scores of the three groups at 12 and 24 h did not show any significant difference. CONCLUSIONS Both sevoflurane and isoflurane attenuated inflammatory response, lipid peroxidation, and oxidative stress. Furthermore, sevoflurane was more effective in modulating sepsis induced inflammatory response at the chosen concentration in sepsis model.

Comparison of intravenous and peritonsillar infiltration of tramadol for postoperative pain relief in children following adenotonsillectomy

Background and objective The aim of this study was to compare the postoperative analgesic efficacy and side-effects of intravenous tramadol with peritonsillar infiltration of tramadol in children undergoing adenotonsillectomy. Methods Sixty-six children were randomized into two groups: group I received 2 mg kg−1 tramadol intravenously and group II received 2 mg kg−1 tramadol in 2 ml of normal saline (1 ml per tonsil) via peritonsillar infiltration. Modified Hannallah pain scale, nausea, vomiting, bleeding, rescue analgesia, sedation and Aldrete scores were recorded at the 1st, 15th, 30th and 60th minute postoperatively. The Aldrete score was used to determine the postanaesthesia care unit discharge criteria. Patients were evaluated for the analgesic requirement, nausea and vomiting, bleeding and sedation. Results There were no differences between groups during the first 1 h. In the postanaesthesia care unit, groups I and II had comparable pain scores that were not statistically significant (P > 0.05). But during the first 24 h the additional analgesic requirement of group I (141.81 mg) was more than group II (83.63 mg) (P = 0.002). Pain scores in the postoperative ward at 6, 12 and 24 h were significantly higher in group I than in group II (P < 0.001). Also four patients (12.12%) from group I and one patient (3.05%) from group II had nausea and vomiting in the postanaesthesia care unit and none of the patients had rescue analgesics. There were no differences between groups regarding nausea and vomiting, sedation and bleeding in the postoperative ward. Conclusion In adenotonsillectomy cases, peritonsillar infiltration of tramadol maintains efficient pain relief with lower incidence of nausea and vomiting.

Thoracic epidural bupivacaine attenuates inflammatory response, intestinal lipid peroxidation, oxidative injury, and mucosal apoptosis induced by mesenteric ischemia/reperfusion.

BACKGROUND: We conducted this study to evaluate the effects of thoracic epidural anesthesia (TEA) on inflammatory response, lipid peroxidation, and oxidative stress in a rat model of mesenteric ischemia/reperfusion (I/R). METHOD: Rats were divided into 4 groups: sham group (n = 6; sham laparotomy), control group (n = 6; I/R), bupivacaine group (n = 6; mesenteric I/R and 20 &mgr;L/h 0.5% bupivacaine), and saline group (n = 6, mesenteric I/R and 20 &mgr;L/h 0.9% saline). I/R injury was established by occluding the superior mesenteric artery for 1 hour followed by 12 hours reperfusion. Blood gas, tumor necrosis factor-&agr;, interleukin-6, interleukin-1&bgr;, glutathione peroxidise, superoxide dismutase, catalese, myeloperoxidase concentrations, immunohistochemical examinations (intracellular adhesion molecule-1), apoptosis determination, and wet/dry ratio of intestinal edema were determined. RESULTS: Bupivacaine significantly decreased the cytokine, malondialdehyde, and myeloperoxidase levels and increased the antioxidant enzyme levels. Wet/dry ratio comparison showed a significant decrease in the bupivacaine (2.88 ± 0.17) group in comparison with control (5.45 ± 0.67) and saline (5.87 ± 0.17) groups. The intestinal injury score was significantly decreased in rats in the epidural bupivacaine (2 [1–2]) infusion group in comparison with rats in the control (3 [2–3]) and saline (3 [2–4]) groups. Bupivacaine (63%) caused a significant decrease in the percentage of apoptotic cells in comparison withcontrol (85%) only. ICAM-1 levels in the bupivacaine (27.4 ± 7.1) group decreased in comparison with control (12.3 ± 7.4) and saline (24.9 ± 3.2) groups. CONCLUSION: This study demonstrated that epidural bupivacaine attenuates the mesenteric I/R-related inflammatory response and intestinal damage.

A comparison of fentanyl with tramadol during propofol-based deep sedation for pediatric upper endoscopy.

Aim:  This study was conducted to compare the efficacy and safety of tramadol with those of fentanyl and to evaluate the impact of age in pediatric patients undergoing upper gastrointestinal endoscopy (UGIE).

Preincisional local infiltration of tramadol at the trocar site versus intravenous tramadol for pain control after laparoscopic cholecystectomy.

STUDY OBJECTIVE To compare the effects of preoperative intravenous (IV) tramadol and preoperative tramadol infiltration of trocar sites on postoperative pain and postoperative nausea and vomiting (PONV) after laparoscopic cholecystectomy. DESIGN Prospective, randomized study. SETTING Operating room, recovery room, and surgical ward. PATIENTS 70 ASA physical status 1 and 2 patients, aged 20-70 years, scheduled for elective laparoscopic cholecystectomy. INTERVENTIONS In Group I, patients received IV 2.0 mg/kg of tramadol; in Group II, trocar insertion points were infiltrated with 2.0 mg/kg of tramadol in 20 mL of 0.9% NaCl. MEASUREMENTS Pain scores, sedation scores, postoperative analgesic requirement, and PONV were recorded at 0 and 30 minutes and one, three, 6, 12, and 24 hours. At 30 minutes and one hour, pain localization (incisional or diffuse abdominal) was also recorded. MAIN RESULTS Visual analog scale scores at 30 minutes were significantly lower in Group II [3 (0-7)] than Group I [6 (3-8)] (P < 0.001). In Group I, 91.4% of patients received sodium diclofenac, while 68.6% of Group II patients received sodium diclofenac (P = 0.002). The time to first analgesic requirement was significantly lower in Group II (P = 0.004). At the 30-minute measurement time, a significant difference was recorded between the groups in incisional pain (P < 0.001). There was also a significant difference between groups in the frequency of PONV. CONCLUSIONS Trocar site infiltration of tramadol improves early postoperative pain and decreases PONV.

Administration of Chlorella sp. microalgae reduces endotoxemia, intestinal oxidative stress and bacterial translocation in experimental biliary obstruction

RATIONALE Endotoxemia has long been documented in obstructive jaundice, and altered intestinal barrier function is considered to be one of the important mechanisms for this phenomenon. The aim of this study was to investigate the role of different microalgae (Chlorella sp. and Spirulina sp.) extracts in intestinal barrier function and oxidative stress in experimentally jaundiced rats. METHODS A total of 60 male wistar rats were randomly divided into four groups of 15 each: I, sham operated; II, bile duct ligation (BDL); III, BDL+Chlorella sp.; IV, BDL+Spirulina sp. Rats were fed rat chow or microalgae extracts supplemented enteral diet ten days after sham operation or BDL. Main outcome measures were endotoxin concentrations in plasma, evidence of bacterial translocation (BT) in mesenteric lymph nodes (MLNs) and liver, oxidative stress, and histology. RESULTS Compared to the group I, a significant increase in contamined MLNs, liver, and spleen samples and increased endotoxemia were noted in group II (P<0.01) but were significant reduced in group III (P<0.05). There was no significant difference in BT rate between the group II and group IV (P>0.05). Moreover, Chlorella sp. administration protected in jaundiced rats against oxidative stress, as demonstrated by reduction of intestinal lipid peroxidation, increase of the antioxidant reduced glutathione (GSH), and decrease of the oxidized glutathione (GSSG). The intestinal mucosa in control rats was atrophic with significantly decreased villous density and total mucosal thickness. Chlorella sp. caused a significant reduction in villous atrophy compared with controls. CONCLUSIONS Chlorella sp. microalgae supplemented enteral diet has significant protective effects on intestinal mucosa barrier in obstructive jaundice, and reduces intestinal translocation of bacteria and endotoxin.

Effects of steep Trendelenburg position and pneumoperitoneum on middleear pressure in patients undergoing robotic radical prostatectomy

BACKGROUND/AIM The aim of this study was to quantify the changes in middle ear pressure (MEP) during robot-assisted radical prostatectomy (RARP). MATERIALS AND METHODS Thirty patients undergoing RARP were included in this study. MEP was obtained at the following time points: awake (T1), postintubation (T2), pneumoperitoneum + 1 h of Trendelenburg position (T3), pneumoperitoneum + 2 h of Trendelenburg position (T4), pneumoperitoneum + 3 h of Trendelenburg position (T5), desufflation + supine position (T6), and 1 h after extubation in the postanesthesia care unit (T7). Heart rate, mean arterial pressure (MAP), peak airway pressure (PAP), tidal volume, minute ventilation, EtCO2, and blood gas values were recorded. RESULTS MEP was significantly higher at T4, T5, T6, and T7 as compared to T1 values. PAP values were significantly increased at T3, T4, and T5 compared to T2. MAP values at T3, T4, and T5 were significantly higher compared to T1. PaCO2 increased significantly at T4, T5, and T6 and pH decreased significantly at T4 and T5 when compared to T2. CONCLUSION The combination of steep Trendelenburg position and pneumoperitoneum during RARP caused a significant increase in MEP, PaCO2, and EtCO2 levels. This propensity for increased MEP may cause problems in patients with preexisting ear disease.

Sevoflurane exerts brain-protective effects against sepsis-associated encephalopathy and memory impairment through caspase 3/9 and Bax/Bcl signaling pathway in a rat model of sepsis:

Objective We compared the effects of sevoflurane and isoflurane on systemic inflammation, sepsis-associated encephalopathy, and memory impairment in a rat sepsis model of cecal ligation and puncture (CLP)-induced polymicrobial peritonitis. Methods Twenty-four rats were assigned to sham, CLP, CLP + sevoflurane, and CLP + isoflurane groups. At 72 hours after CLP, the rats underwent behavior tests. Serum cytokines were evaluated. Brain tissue samples were collected for determination of glutathione peroxidase (GPX), superoxide dismutase (SOD), and catalase; the wet/dry weight ratio; myeloperoxidase (MPO) and malondialdehyde (MDA); apoptotic gene release; and histologic examinations. Results The MPO level, wet/dry weight ratio, and histopathology scores were lower and the Bcl2a1 and Bcl2l2 expressions were upregulated in both the CLP + sevoflurane and CLP + isoflurane groups compared with the CLP group. The interleukin-6, interleukin-1β, MDA, and caspase 3, 8, and 9 levels were lower; the GPX, SOD, Bax, Bcl2, and Bclx levels were higher; and non-associative and aversive memory were improved in the CLP + sevoflurane group compared with the CLP + isoflurane group. Conclusion Sevoflurane decreased apoptosis and oxidative injury and improved memory in this experimental rat model of CLP. Sevoflurane sedation may protect against brain injury and memory impairment in septic patients.