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More rapid, and specific molecular diagnostic methods are required to understand the epidemiology of tuberculosis in the population and to establish effective control measures. Molecular epidemiologic studies about Mycobacterium tuberculosis are yet limited in Turkey. Cukurova (Eastern Mediterranean part of Turkey) region is of special importance in terms of tuberculosis epidemiology due to its neighbourhood countries and relatively high number of immigrants to that area. This study was aimed to determine the genotypic characteristics of M.tuberculosis strains isolated from pulmonary tuberculosis patients in Cukurova region, by spoligotyping and 12 loci MIRU-VNTR (Mycobacterial Interspersed Repetitive Unit- Variable Number Tandem Repeats) methods. A total of 467 M.tuberculosis strains isolated from patients with pulmonary tuberculosis admitted to 20 hospital/dispansery in seven different provinces (Adana, Mersin, Osmaniye, Antakya, Gaziantep, Sanliurfa, Kahramanmaras) at Cukurova region between January 2007-June 2010, were included to the study. Genotypic identification was done by spoligotyping and 12 loci MIRU-VNTR methods. M.tuberculosis complex strains were isolated from different samples (sputum, bronchoalveolar lavage and biopsy material) by MGIT 960-TB (BD Diagnostics, USA) liquid culture method in Regional Tuberculosis Laboratory. Spoligotyping analysis revealed that 443 (94.9%) of the strains were clustered in 21 groups while 24 (5.1%) of the isolates were described as orphan strains according to SpolDB4 database. The most common families were T1 genotype seen in 239 (51.9%) strains and LAM7 TUR genotype seen in 54 (11.5%) strains. Six (1.3%) strains isolated from one province were multidrug resistant strains and belonged to Beijing family. Combination of spoligotyping with 12- locus MIRU-VNTR divided the T1 family into 7 clusters of which members ranged from 2-158. Twenty one isolates showed unique pattern. According to this study, T1 family is the most common genotype among M.tuberculosis strains in Cukurova, Turkey and the prevalence of M.tuberculosis Beijing strains was 1.3%, detected only in one province (Sanliurfa). Active surveillance studies are necessary to follow the regional dissemination of M.tuberculosis genotypes and establish effective precautions to prevent the spread of especially drug resistant strains.

Background: Postoperative nausea and vomiting (PONV) are some of the most-common and undesirable adverse effects after surgery performed under general anesthesia. We investigated the prophylactic value of dexamethasone as an alternate to ondansetron or metoclopramide to prevent PONV after gynecologic surgery., Material/methods: One hundred sixty ASA I-II patients scheduled for elective gynecologic surgery were enrolled. Before induction of anesthesia, patients were randomly allocated to receive intravenously dexamethasone (8 mg) in group D, ondansetron (4 mg) in group O, metoclopramide (10 mg) in group M, and saline (2 mL) in group P. Total incidence of nausea and vomiting, rescue antiemetic requirement, pain scores, and any adverse effects were recorded at 3 observational periods (0-2 hours, 2-12 hours, and 12-24 hours)., Results: Total rates of PON, POV, and PONV were significantly higher in group P at 0-2 hours and 2-12 hours compared with group D, O, and M (P<.05). There was no difference in PON, POV, and PONV among D, O, and M groups. None of the groups differed in PONV in the subsequent 12-24 hours. Number of patients requiring rescue antiemetic was significantly higher in group P than the other groups at 0-2 hours (10%, 10%, 15%, and 45% in group D, O, M, and P) (P<.05)., Conclusions: Prophylactic IV dexamethasone 8 mg significantly reduces the incidence of PONV in gynecologic surgery. At this dosage, dexamethasone is as effective as ondansetron 4 mg and metoclopramide 10 mg, and is more-effective than placebo.

Background: Intrathecal morphine has been used in hopes of providing long-lasting postoperative analgesia in patients after cardiac surgery. The aim of this study was to evaluate the effects of 7 micro/kg intrathecal morphine administration in coronary bypass surgery in the postoperative period., Methods: We conducted a prospective, randomized, blinded, and controlled study. Twenty-three patients, who underwent primary elective coronary bypass surgery, were randomly allocated to receive morphine 7 micro/kg intrathecally, before the induction of general anesthesia (Group M, n = 12) or no intrathecal injection (Group C, n = 11). Pain scores, determined by visual analogue scale (VAS), were recorded immediately after extubation upon admission to the intensive care unit (ICU), at the 2nd, 4th, 6th, and 18th hour after extubation. Pethidine was administered if the patient's VAS > or = 4 and consumption was recorded. Extubation time and ICU length of stay were also recorded., Results: VAS scores were lower in the Group M at each measured time than the control group (p = 0.016, 0.023, 0.004, 0.0001, and 0.001, respectively). According to the VAS scores, pethidine requirement was lower in the Group M than the control (p = 0.001). Extubation time (3.58 +/- 1.57 vs. 4.86 +/- 1.38 hours, p = 0.045) and ICU length of stay (16.25 +/- 2.70 vs. 19.30 +/- 2.45 hours, p = 0.014) were also significantly shorter in the Group M than the control group. No significant complications were seen in this group of patients., Conclusions: Intrathecal morphine provided effective analgesia, earlier tracheal extubation and less ICU length stay after on-pump coronary bypass surgery. The influence on ICU length of stay requires further evaluations.

Background and Objective: Levosimendan has a cardioprotective action by inducing coronary vasodilatation and preconditioning by opening KATP channels. The aim of this study was to determine whether levosimendan enhances myocardial damage during hypothermic ischaemia and reperfusion in isolated rat hearts., Methods: Twenty-one male Wistar rats were divided into three groups. After surgical preparation, coronary circulation was started by retrograde aortic perfusion using Krebs-Henseleit buffer solution and lasted 15 min. After perfusion Group 1 (control; n = 7) received no further treatment. In Group 2 (non-treated; n = 7), hearts were arrested with cold cardioplegic solution after perfusion and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. In Group 3 (levosimendan treated; n = 7), levosimendan was added to the buffer solution during perfusion and the hearts were arrested with cold cardioplegic solution and subjected to 60 min of hypothermic global ischaemia followed by 30 min reperfusion. At the end of the reperfusion period, the hearts were prepared for biochemical assays and for histological analysis., Results: Tissue malondialdehyde levels were significantly lower in the levosimendan-treated group than in the non-treated group (P = 0.019). The tissue Na+-K+ ATPase activity was significantly decreased in the non-treated group than in the levosimendan-treated group (P = 0.027). Tissue myeloperoxidase (MPO) enzyme activity was significantly higher in the non-treated group than in the levosimendan-treated group (P = 0.004). Electron microscopic examination of the hearts showed cardiomyocytic degeneration at the myofibril, mitochondria and sarcoplasmic reticulum in both non-treated and levosimendan-treated groups. The severity of these findings was more extensive in the non-treated group., Conclusions: Treatment with levosimendan provided better cardioprotection with cold cardioplegic arrest followed by global hypothermic ischaemia in isolated rat hearts.

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.

The purpose of this study was to evaluate the impact of the Glasgow Coma Scale (GCS), Acute Physiology and Chronic Health Evaluation (APACHE) II and Simplified Acute Physiology Score (SAPS) II scoring systems for organophosphate poisoning (OPP) in an intensive care unit (ICU). The following data were collected on all consecutive patients who were admitted to the ICU between June 1999 and December 2004. Demographic data, GCS, APACHE II and SAPS II scoring systems were recorded. Predicted mortality was calculated using original regression formulas. Standardized mortality ratio (SMR) was computed with 95% confidence intervals (CI). The sensitivity and specificity for each scoring system were evaluated by calculating the Area Under the Receiver Operating Characteristic Curves. The actual mortality in OPP was 21.9%. Predicted mortality by all systems was not significantly different from actual mortality [SMR and 95% CI for GCS: 1.00 (0.65 1.35), APACHE II: 0.87 (0.54-1.03), SAPS II: 1.40 (0.98-1.82)]. The area under the ROC curve for APACHE II is largest, but there is no statistically significant difference when compared with SAPS II and GCS (GCS 0.900 +/- 0.059, APACHE II 0.929 +/- 0.045 and SAPS II 0.891 +/- 0.057). In our ICU group of patients, in predicting the mortality rates in OPP, the three scoring systems, which are GCS, APACHE II and SAPS II, had similar impacts; however, GCS system has superiority over the other systems in being easy to perform, and not requiring complex physiologic parameters and laboratory methods.

In this study, histopathological and biochemical changes due to chronic usage of morphine or tramadol in liver and kidney were assessed in rats. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4, 8, 10 mg/kg/day in the first, second and the third ten days of the study, respectively. Tramadol group (n = 10), received the drug intraperitoneally at doses of 20, 40 and 80 mg/kg/day in the first, second and the third ten days of the study, respectively. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatinin, blood urea nitrogen (BUN) and malondialdehyde (MDA) levels were measured in the serum. Liver and kidney specimens were evaluated by light microscopy. Serum ALT, AST, LDH, BUN and creatinin levels were significantly higher in morphine group compared to the control group. Serum LDH, BUN and creatinin levels were significantly increased in the morphine group compared to the tramadol group. The mean MDA level was significantly higher in morphine group compared to the tramadol and control groups (P < 0.05). Light microscopy revealed severe centrolobular congestion and focal necrosis in the liver of morphine and tramadol groups, but perivenular necrosis was present only in the morphine group. The main histopathologic finding was vacuolization in tubular cells in morphine and tramadol groups. Our findings pointed out the risk of increased lipid peroxidation, hepatic and renal damage due to long term use of opioids, especially morphine. Although opioids are reported to be effective in pain management, their toxic effects should be kept in mind during chronic usage.

Background: Low muscle glutamine levels during sepsis are associated with reduced protein synthesis and elevated protein breakdown, in particular myofibrillar protein breakdown. Thus, in a cecal ligation and puncture (CLP)-induced sepsis model in the rat, we hypothesized that glutamine pretreatment would protect the diaphragm muscle function., Methods: Eighty-four male Wistar rats weighing between 180 g and 200 g received standard amino acid solution 1.2 g kg(-1) per day intraperitoneally (IP) or standard amino acid solution 1.2 g kg(-1) per day plus alanyl-glutamine (GLN) 0.25 g kg(-1) per day (IP) during the first 6 days of the experiment. On the seventh day, CLP or sham procedures were applied. The sham and CLP groups were equally divided into 3 subgroups according to the termination of the experiment, which took place at either the 24th hour, 48th hour, or 72nd hour. After the compound muscle action potentials (CMAP) were recorded from the diaphragms of the rats at these selected times, they were decapitated under ketamine/xylazine anesthesia, and diaphragms were harvested for biochemical and histopathological examination., Results: The mean area and amplitude of CMAP were significantly larger in sham+GLN groups when compared with CLP and CLP+GLN groups at all times (p < .05). Diaphragm Ca+2 -ATPase levels were found to be significantly decreased in CLP group at all times compared to sham groups (p < .05). Diaphragm reduced glutathione levels were significantly higher in sham+GLN groups when compared with CLP and CLP+GLN groups at all times (p < .05). In histopathologic assessment, moderate neutrophil infiltration, which was observed in CLP48, was significantly reduced with alanyl-glutamine supplementation in CLP+GLN48 group (p < .05)., Conclusions: This study showed that glutamine pretreatment did not improve diaphragm muscle function, but prevented the biochemical and histopathological changes in diaphragmatic muscle in CLP-induced sepsis. However, further studies are needed to clarify whether a higher dose of glutamine supplementation might protect the diaphragmatic muscle functions.

Histopathologic changes in rat brain due to chronic use of morphine and/or tramadol in progressively increased doses were investigated in this study. Thirty male Wistar rats (180-220 g) were included and divided into three groups. Normal saline (1 ml/kg) was given intraperitoneally as placebo in the control group (n = 10). Morphine group (n = 10) received morphine intraperitoneally at a dose of 4 mg/kg/day for the first 10 days, 8 mg/kg/day between 11-20 days, and 12 mg/kg/day between 21-30 days. The tramadol group (n = 10) received the drug intraperitoneally at doses of 20, 40, and 80 mg/kg/day in the first, second, and the third 10 days of the study, respectively. All rats were decapitated on the 30th day and the brain was removed intact for histology. The presence and the number of red neurons, which are a histologic marker of apoptosis, were investigated in the parietal, frontal, temporal, occipital, entorhinal, pyriform, and hippocampal CA1, CA2, CA3 regions. Red neurons were found in morphine and tramadol groups but not in the control group. The total number of red neurons was not different in morphine and tramadol groups, but the numbers of red neurons were significantly higher in the temporal and occipital regions in tramadol group as compared with the morphine group (p < .05). In conclusion, chronic use of morphine and/or tramadol in increasing doses is found to cause red neuron degeneration in the rat brain, which probably contributes to cerebral dysfunction. These findings should be taken into consideration when chrome use of opioids is indicated.

Since oleic acid (OA) induces morphologic and cellular changes similar to those observed in human acute lung injury (ALI) and acute respiratory distress syndrome, it has become a widely used model to investigate the effects of several agents on pathogenesis of lung injury. The antioxidant and anti-inflammatory properties of N-acetylcysteine (NAC) has been documented in many lung injury models. 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 labelled Sham, NAC, OA, Pre-OA-NAC and Post-OA-NAC were determined. ALI was induced by intravenous 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 h after OA infusion. In both of the NAC treatment groups' blood and tissue samples were collected 4 h after OA infusion, independent from the time of NAC infusion. The MPO activity, MDA and 3-NT levels in lung homogenates were found to be increased in OA group and the administration of NAC significantly reduced tissue MPO, MDA and 3-NT levels (p = 0.0001) Lung histopathology was also affected by NAC in this OA-induced experimental lung injury model.

Objectives: To examine in a prospective, randomized, double-blind, placebo-controlled study the analgesic effect of periprostatic nerve block and/or intravenous synthetic opioid administration during a 12-core prostate biopsy., Patients and Methods: Patients were prospectively randomized to receive unilateral periprostatic lidocaine administration and/or intravenous synthetic opioid (meperidine or tramadol) administration. Placebo groups received sterile normal saline. Unilateral infiltration was performed and biopsy was begun on this side. The degree of pain was recorded using the visual analog scale/numeric analog scale (VAS/NAS) score before the procedure, during probe introduction into the rectum, during unilateral periprostatic nerve blockade, during the first 6-core biopsy and during the second 6-core biopsy, and 30 min after biopsy completion., Results: Most of the patients had mild or moderate pain (VAS/NAS <6) during the actual biopsy procedure. However, no significant differences existed between the groups with regard to the pain scores at any time (p > 0.05). Compared with pain scores, no significant differences existed between the first 6-core (blocked side) and second 6-core biopsies (p > 0.05)., Conclusion: Periprostatic lidocaine infiltration and/or intravenous synthetic opioid analgesics are not beneficial in significantly reducing pain during biopsy. We think that most of the patients do have pain during biopsy, however the intensity of pain is tolerable and does not require analgesics., (Copyright 2004 S. Karger AG, Basel)

Purpose: To investigate the effect of N-acetylcysteine on preventing pump-induced oxidoinflammatory response during cardiopulmonary bypass (CPB)., Methods: Forty patients undergoing coronary artery bypass grafting (CABG) were randomly divided into a study group (n = 20), given 50 mg kg(-1) N-acetylcysteine intravenously for 3 days, and a control group (n = 20) given saline. Serum samples were collected for measurement of myeloperoxidase (MPO), malondialdehyde (MDA), interleukin-6, Alpha1-acid glycoprotein (AAGP), and C-reactive protein (CRP) during surgery and postoperatively., Results: The MPO and MDA values showed a similar pattern during and after CPB in the study group, with significantly less variance than in the control group. Interleukin-6 showed similar patterns in the two groups, but the data from 30 min after the start of CPB and from 6 h post-CPB were significantly different. The AAGP and CRP values were both elevated during CPB in the two groups without a significant difference, but 6 and 24 h post-CPB, the values were significantly higher in the control group than in the study group., Conclusions: N-Acetylcysteine decreased pump-induced oxidoinflammatory response during CPB, suggesting that it could be a novel therapy for assisting in the prevention of CBP-induced oxidoinflammatory damage.

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.

Recent experimental studies have described protective effect of ischemic preconditioning (IPC) on ischemia-reperfusion (I/R) injury of the intestine. We hypothesize that to reach a new point of view on the effect of IPC in intestinal barrier function, the relationship between I/R-induced mucosal injury and apoptosis must first be clarified. The present study was undertaken to investigate the role of IPC on intestinal apoptosis and probable contributions of bcl-2 expression to this process. We also investigated the effect of intestinal IPC on ileal malondyaldihyde levels. Forty-four male Wistar rats were randomized into four groups each consisting of 11 rats: sham-operated control, I/R group (30 min of superior mesenteric artery occlusion), IPC-I/R group (10 min of temporary artery occlusion prior before an ischemic insult of 30 min), and IPC alone group (10 min of preconditioning). Twenty-four hours later, ileum samples were obtained. Ileal malondyaldihyde levels were increased in the I/R group (31.9 +/- 18.8 vs. 106.8 +/- 39.8) but not in the IPC alone and IPC-I/R groups (38.1 +/- 13.6 and 44.7 +/- 12.7; P < 0.01). The number of apoptotic cells was significantly lower in IPC-I/R group than that of I/R group, and these findings were further supported by DNA laddering and M30 findings. Diminished bcl-2 expression observed in the ileal specimens of I/R group was prevented by IPC. Our results indicate that IPC may provide a protective effect on ileal epithelium and that this effect is probably the result of a significant increase in the expression of bcl-2 after the insult. The reversal of apoptosis by IPC might help preserving the vitality of intestinal structures that have a critical function, cessation of which often leads to multiorgan dysfunction syndrome.

Effect of ornithine which is known to inhibit L-arginine uptake via cationic amino acid transport system has been tested, and compared to aminoguanidine, an iNOS inhibitor in lypopolysaccharide (LPS)-induced endotoxemia in rats. Serum nitrite/nitrate and malondialdehyde (MDA) level have been measured, and ileal histology has also been examined. Endotoxin increased serum nitrite/nitrate and MDA levels from 15.7+/- 2.4 micromol/ml and 2.1 +/-0.2 nmol/ml to 23.1 +/- 1.0 micromol/ml and 5.2+/- 0.3 nmol/ml (both P<0.05), respectively. In addition, LPS caused ileal degeneration. L-ornithine (500 mg/kg) did not improve septic manifestations, i.e., serum nitrite/nitrate and MDA levels did not differ from those in endotoxemia. Neither does it have an improving action on ileal histology. However, higher dose of L-ornithine (2,500 mg/kg) lowered the increased level of nitrite/nitrate and MDA by LPS. Moreover, it restored ileal histology from grade 3 (median) to 0 (median) (P<0.05). On the other hand, aminoguanidine (100 mg/kg) normalized serum nitrite/nitrate and MDA levels but not ileal histology in endotoxemic rats. In conclusion, high dose of L-ornithine could improve endotoxemic parameters in LPS-treated rats.

Apoptotic loss of parenchymal cells may lead to organ dysfunctions in critically ill patients with septic states. As an antioxidant, the protective effects of N-acetylcysteine (NAC) are documented in many experimental and clinical studies. In this experimental study, we investigated the role of chronically used NAC in septic lung injury on a cecal ligation and puncture (CLP) model. To evaluate this, 30 male Wistar rats were randomly divided into four groups as sham (n = 7), CLP (n = 8), sham + NAC (n = 7) and CLP + NAC (n = 8) groups. NAC was administered 150 mg kg(-1) day through intramuscular route beginning 6 h after the operations and lasting for a period of 1 week. One week later, histopathology and epithelial apoptosis were assessed by hematoxylin-eosin and immunohistochemically by M30 and caspase 3 staining to demonstrate septic lung injury. Additionally, lung tissue myeloperoxidase (MPO) activity, malondialdehyde (MDA), and nitrite/nitrate levels were measured. The MPO activity and MDA levels in lung homogenates were found to be increased in CLP group and the administration of NAC prevented their increase significantly (P < 0.05). However, there were no significant differences among the groups regarding nitrite/nitrate levels. The number of apoptotic cells was significantly lower in CLP+NAC group than CLP group, and this finding was supported by M30 and caspase 3 expression in lung (P < 0.05). Lung histopathology was also protected by NAC in CLP-induced sepsis. In conclusion, the chronic use of NAC inhibited MPO activity and lipid peroxidation, which resulted in reduction of apoptosis in lung in this CLP model. Because lung tissue nitrite/nitrate levels did not change significantly, organs other than the lungs may be responsible for producing the increased nitric oxide during sepsis. The chronic use of NAC needs further investigation for its possible antiapoptotic potential in septic states besides its documented antioxidant and antiinflammatory effects.

Ischemic preconditioning (IPC) was first demonstrated in the heart, but this protective effect has been also recently described in the intestine. The aim of this study was to determine the effects of intestinal ischemic preconditioning on the morphology of intestine and bacterial translocation. Twenty-four male Wistar rats weighting 250 to 300 g were randomized into three groups. A control group of rats (n = 8) were subjected laparotomy. In an ischemic group (n = 8), laparotomy was performed and the superior mesenteric artery was occluded by an atraumatic clamp for 30 min. In the preconditioned group (n = 8), before the ischemia-reperfusion (I/R) period (as in ischemic group), rats were subjected to an initial 10 min of intestinal ischemia and 10 min of reperfusion. Twenty-four hours later, to evaluate whether the I/R induced intestinal injury and bacterial translocation (BT), tissue and blood samples were collected, and liver, spleen, and mesenteric lymph node specimens were obtained under sterile conditions for microbiological analysis. Samples of ileum were removed for both biochemical and histopathological evaluation. In the I/R group, the incidence of bacteria-isolated mesenteric lymph nodes, spleen, liver, and blood was significantly higher than other groups (P < 0.05). IPC prevented I/R-induced BT and it significantly reduced the I/R-induced intestinal injury (P < 0.05). Increased inducible nitric oxide (NO) synthase (iNOS) expression observed on the ileal specimens of the I/R group was found to be prevented by IPC. Our data suggest IPC as a key factor that reduces BT and iNOS activation in intestinal I/R. This is the first study showing that intestinal IPC blocks the cascade of events that causes BT and intestinal injury that may lead to sepsis.

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<0.05). Selenium supplementation prevented I/R-induced BT and significantly reduced the I/R-induced intestinal injury (P<0.05). Tissue MDA levels from the ileum specimens of selenium-treated rats were significantly lower than that of the I/R group (P<0.05). Our results provide evidence that the relationship between BT and lipid peroxidation in intestinal tissue is crucial. Selenium pretreatment reduces lipid peroxidation which contributes to the maintenance of intestinal mucosal integrity.