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Glutamate neurotoxicity has been implicated in the pathophysiology of cerebral ischemia-reperfusion injury. Therefore, we investigated the effect of glutamate receptor antagonist riluzole in a rabbit model of warm cerebral ischemia-reperfusion. A total of 16 New Zealand rabbits were randoml

Recently, most studies reported magnesium as a N-methyl-d-aspartate receptor antagonist and its analgesic and perioperative anaesthetic effects have been discussed with central desensitization pathway. We investigated the effects of caudal ropivacaine plus magnesium and compared with ropivacaine alone on postoperative analgesia requirements. After hospital ethic committee’s consent, 60 patients (ASA I-II, 2–10 years old) who had lower abdominal or penoscrotal surgery were enrolled in the study. After general anaesthesia induction, caudal blockage was applied. Patients were randomly assigned in two groups. Ropivacaine 0.25% was administered to Group R (n = 37), ropivacaine 0.25% plus 50 mg magnesium to Group RM (n = 23) in 0.5 ml kg−1 volume. Postoperative analgesia level was recorded at 15 min and 1, 2, 3, 4, 6 h by using Paediatric Objective Pain Scale (POPS) and The Children’s Hospital of Eastern Ontoria Pain Scale (CHEOPS). Postoperative motor blocks were evaluated with Modified Bromage Motor Block Scale. According to demographic characteristics, there were no significant differences between the two groups (P > 0.05). POPS, CHEOPS, Bromage Motor Scales, analgesia duration and adverse effects were similar in Group R and Group RM. It has been shown that addition of magnesium as an adjuvant agent to local anaesthetics for caudal analgesia has no effect on postoperative pain and analgesic need.

Background and objective: Adequate relief of pain after tonsillectomy is a common problem. We compared meperidine and tramadol when given at induction of anaesthesia with respect to their effects on postoperative pain relief and emergence characteristics after adenotonsillectomy in children. Methods: Fifty children aged 4-7 yr undergoing tonsillectomy were randomly assigned to receive either tramadol 1 mg kg -1 (n = 25) or meperidine 1 mg kg -1 (n = 25) before commencement of the surgical procedure. Anaesthesia was induced with propofol (with cis-atracurium for muscle relaxation) and maintained with sevoflurane in oxygen and nitrous oxide. Postoperative pain was scored by a blinded observer using a facial pain scale in the recovery room at 0 (at arrival of the patient in the postoperative care unit) and at 10, 20 and 45 min thereafter. Agitation scores were also assessed by the same observer at 0 min. Heart rate and mean arterial pressure were recorded at regular intervals. The time to recovery to spontaneous respiration and the incidence of postoperative nausea and vomiting were noted. Results: Facial pain scale scores were increased in the tramadol group at 0, 10 and 20 min (P < 0.05). No difference was observed in scores at the 45th min postoperation. Agitation scores were higher in the tramadol group than in the meperidine group. No statistical difference was found between the two groups. Heart rates and mean arterial pressures were similar in both groups. The time to recovery to spontaneous respiration was delayed with meperidine compared with tramadol (P < 0.05). The incidence of nausea and vomiting was not statistically different between groups. Conclusions: Meperidine was more effective for pain relief and provides better emergence characteristics than tramadol after tonsillectomy in children.

Protective role of selenium against free radical damage was first demonstrated in the heart and this effect was further questioned in other systems. In the present study, the effects of exogenously administered selenium on intestinal fine morphology, lipid peroxidation, and bacterial translocation (BT) in experimental intestinal ischemia/reperfusion (I/R) model were examined. Thirty-two male Wistar rats weighing 250-300 g were randomized into four groups. Sham group (n=8) underwent laparotomy only. In the I/R group (n=8), laparotomy was performed and the superior mesenteric artery was occluded using an atraumatic microvascular clamp for 30 min. In corresponding selenium-treated groups (n=8 each), sodium selenate was given 0.2 mg kg(-1)day(-1) intraperitoneally (i.p.) for 3 consecutive days, prior to surgery for either laparotomy only or with I/R. Twenty-four hours later, tissue samples from liver, spleen, and mesenteric lymph nodes were obtained under sterile conditions for microbiological analysis and further evaluation of I/R-induced intestinal injury. Ileum samples were fixed in 10% formaldehyde for histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, and liver was significantly higher than other groups (P

Contamination of propofol, in an emulsion formulation, has been associated with infective complications. Local anaesthetics, some of which are known to have antibacterial properties, are frequently added to the solution to reduce pain on injection. We examined the growth rates of E. coli, S. aureus, S. epidermidis and P. aeruginosa in propofol with and without lignocaine 0.1%–2% after incubation for 2, 5 and 24 hours at 37°C. Growth of microorganisms in each solution was compared by counting the number of colony forming units (CFU). Propofol supported the growth of all microorganisms. An increase in the number of CFUs was observed in all drug combinations 2, 5 and 24 hours after inoculation except for S.aureus (P We conclude that lignocaine in recommended clinical doses (0.05%–0.1%) did not exhibit adequate antibacterial activity to prevent infective complications.

PubMed: 11692987 Background: Postoperative pain relief after major surgery cannot be achieved with opioids alone in all patients without respiratory depression or other significant drawbacks. Modern medical practice, therefore, dictates the use of alternative analgesic agents as an adjunct or substitute to minimize the deleterious effects and to facilitate an earlier return to work and daily activities. Diclofenac and metamizol inhibit prostaglandin synthesis, thus attenuate the peripheral nociceptive sensitization caused by the surgical trauma. This investigation was conducted to determine the potency of diclofenac compared with metamizol in the control of postoperative pain after various plastic surgical operations under general anesthesia. Methods: A multiple-dose, randomized, double-blind clinical trial composed of one hundred and sixty-six patients was conducted. Group M patients received 1 g intramuscular metamizol (every 8 hours) and Group D patients received 75 mg intramuscular diclofenac (every 12 hours). Additional analgesia requirements were recorded and meperidine was used as the complementary analgesic when needed. Plain was assessed by visual analogue scores. Platelet count and bleeding time analyses were performed preoperatively and on the first postoperative day. Results: Metamizol decreased the additional analgesia requirement during the 18 hours following surgery. This was also associated with significantly lower pain scores. There was no significant difference between the patients receiving either metamizol or diclofenac in terms of pain scores, additional request for analgesia and frequency of side effects from the 18th until the 48th hour postoperatively. However, the use of diclofenac was associated with reduced side effects, though a reduction in platelet number and prolongation of bleeding time was noted in the majority of the patients receiving diclofenac. Conclusions: Metamizol is significantly superior to diclofenac for the reduction of postoperative pain after plastic surgery in the first 18 hours after plastic surgery procedures and reduces the need for additional analgesia.

Ethyl pyruvate (EP) is a pyruvate derivative that has been reported to improve survival, to decrease proinflammatory cytokine expression (including high mobility group box-1) and to ameliorate organ dysfunction in animals who have lethal sepsis or were subjected to hemorrhagic shock. We examined the potential protective effects of EP administered after multi-trauma on lung oxidative damage and apoptosis in a rat model with delayed resuscitation.

We have previously demonstrated that following cecal ligation and puncture (CLP) there is an increase in lung epithelial apoptosis in a rat model [1]. On the other hand, it has been shown that the rho/rho kinase pathway is involved in mechanisms of several aspects such as endothelial cell dysfunction and apoptosis. However, the role of rho kinase in the concept of sepsis-induced apoptosis has yet to be elucidated. In this study, to investigate the possible contribution of rho/rho kinase signalling in CLP-induced lung injury, rho kinase expression and the possible protective effect of the administration of an inhibitor of rho kinase, (+)-(R)-trans-4-1-aminoethyl-N-4-pyridyl cyclohexanecarboxamide dihydrochloride monohydrate (Y-27632), has been investigated in rats in this model. Thirty-two male Wistar rats were randomly divided into four groups: (1) sham, (2) CLP, (3) sham + Y27632, (4) CLP + Y27632. Y27632 was administered at 1.5 mg/kg, intaperitoneally, 20 min before performing operations. Twenty-four hours later, histopathology and apoptosis were assessed by H&E and immunohistochemically by caspase-3 to demonstrate septic lung injury. Additionally, expression of rock 1 and rock 2 proteins in lung tissue was analyzed by western blotting, and the contribution of oxidative damage was assessed by measuring the levels of thiobarbituric acid reactive substances (TBARS) and the 3-L-nitrotirozin (3-NT)/total tyrosine ratio. The TBARS and 3-NT/total tirosine ratio levels in lung homogenates were found to be increased (11.05 ± 0.31 vs 29.855 ± 2.87) (0.1485 ± 0.10 vs 0.281 ± 0.05) in the CLP group compared with the sham group, and the administration of Y27632 prevented their increase (8.86 ± 1.87) (0.178 ± 0.02) significantly (P < 0.05). The number of apoptotic cells was significantly lower in the CLP + Y27632 group than CLP group and this finding was supported by caspase-3 expression in the lung. Lung histopathology was also protected by Y27632 in CLP-induced sepsis. Immunoblot experiments revealed the increased expression of active fragment of rock 1 in the CLP group. However, rock 2 expressions were similar in all groups. In conclusion, since CLP induced active fragmentation of rock 1 and rho-kinase inhibitor prevented peroxynitrite-mediated apoptotic lung injury in this CLP-induced sepsis model, this suggests that rho-kinase plays an important role in apoptotic lung injury. Our data indicate that rock 1 or downstream components of this pathway may be potential targets for the development of novel therapies in sepsis.

Background and Goal of Study: Recently most studies reported that magnesium was a N-methyl-D-aspartate (NMDA)-receptor antagonist and its analgesic and perioperative anesthesic effects were discussed with central desentisation pathway. We aimed to study effects of caudal ropivacaine plus magnesium o

Since oleic acid (OA) induces morphologic and cellular changes similar to those observed in human acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), it has become a widely used model to investigate the effects of several agents on pathogenesis of lung injury. The antioxidant, anti-inflammatory and antiapoptotic properties of N-acetylcysteine (NAC) have been documented in many lung injury models [1]. In this study, we evaluated the role of NAC in an OA-induced lung injury model by measuring myeloperoxidase (MPO) activity, malondialdehyde (MDA) and 3-nitrotyrosine (3-NT) levels in lung tissue. Five groups (sham, NAC, OA, pre-OA-NAC and post-OA-NAC) were determined. ALI/ARDS was induced by intravenous (IV) administration of OA. The pre-OA-NAC group received IV NAC 15 min before OA infusion and the post-OA-NAC group received IV NAC 2 hours after OA infusion. In both of the NAC treatment groups, blood and tissue samples were collected 4 hours after OA infusion, independent of the time of NAC infusion. The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in the OA group, and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (P = 0.0001). Lung histopathology was also protected by NAC in this OA-induced experimental lung injury model. In conclusion, the present study demonstrates that oleic acid induces myeloperoxydase activation and consequently increases 3-NT and MDA levels in lung tissue. Our data suggest that elevated 3-NT levels in lung tissue represent the role of excessive formation of peroxynitrite and the efficacy of NAC treatment in the prevention of peroxynitrite-mediated OA-induced lung injury. Due to its antioxidant and anti-inflammatory properties, NAC seems to be a promising agent in treatment of critically ill patients with lung injury states.

Previously it has been shown that ischemic preconditioning could increase the tolerance of intestinal tissue to ischemia [1]. In this study we investigated the effects of pharmacological preconditioning with adenosine infusion on intestinal ischemia/reperfusion (I/R) injury and bacterial translocation. We also evaluated the presence of any additive effects of adenosine administration when used together with ischemic preconditioning.

Recent experimental studies have described the protective effect of ischemic preconditioning (IPC) on ischemia-reperfusion (I/R) injury of the intestine [1,2]. In order to reach a new point of view in the effect of IPC on the intestinal barrier function, the relationship between I/R-induced mucosal injury and apoptosis must be clarified. The present study was undertaken to investigate the relation between IPC and Bcl-2 expression immunohistochemically and apoptosis (by using conventional light microscopy, immunohistochemical staining for cytokeratin 18 [M30 cytodeath Ab], DNA agarose gel electrophoresis) in the intestine. Furthermore, we also investigated the effect of intestinal IPC on serum nitrite/nitrate levels. With approval of the Ethical Committee, 33 male Wistar rats weighing 250-300 g were randomized into three groups. A control group of rats (n = 11) was subjected laparotomy. In an ischemic group (n = 11), laparotomy was performed and the superior mesenteric artery (SMA) was occluded by an atraumatic clamp for 30 min. In the preconditioned group (n = 11), before the ischemia-reperfusion period, rats were subjected to initial 10 min of intestinal ischemia and 10 min of reperfusion. Twenty-four hours later, ileum and blood samples were collected. Nitrite/nitrate levels were measured in the blood samples. Serum nitrate level was found to be increased in the I/R group (16.2 ± 0.9 vs 34.3 ± 4.1) but not in the IPC group (11.3 ± 5.9) (P < 0.05). The numbers of apoptotic cells at 24 hours after I/R were significantly lower in IPC-treated rats. Diminished Bcl-2 expression observed on the ileal specimens of the I/R group was found to be prevented by IPC. Our results indicate that IPC provides a significant protective effect on ileum against I/R injury and that its effect is evidenced by a significant increase in the expression of Bcl-2 following the insult. This study shows that intestinal IPC may block the cascade of events that cause apoptosis that can lead to multiorgan failure. In the future, the use of agents causing Bcl-2 upregulation against the spontaneous I/R attacks as a preservative measure in criticial patients could be seriously considered.