The Relationship Between Small Peritoneal Flap Defects and Postoperative Seroma in TAPP Repair of Inguinal Hernias.

OBJECTIVE: Total abdominal preperitoneal (TAPP) is one of the most frequently used surgical treatment methods in the treatment of inguinal hernia (IH). One of the most common early postoperative complications after hernia repair is seroma/hematoma. In this study, we aimed to study the role of unclosed peritoneal flap defects on the development of postoperative seroma. MATERIAL AND METHODS: The study was performed retrospectively in 2 university hospitals. All patients over the age of 18 years who underwent laparoscopic TAPP surgery in Istanbul Yeni Yüzyil University Gaziosmanpasa Hospital General Surgery Clinic and Van Yüzüncü Yil University Faculty of Medicine General Surgery Clinic between January 1, 2018, and December 31, 2021, were included. Patients were divided into those with peritoneal defects (group 1) and those without (group 2). Whether there was a peritoneal defect or not was compiled from video recordings. In addition, risk factors affecting the development of seroma were determined. RESULTS: A total of 250 patients, 16 (6.4%) women and 234 (93.6%) men, were included in the study. There were bilateral hernias in 35 (14%) patients, and a total of 320 hernias were analyzed in the study. It was determined that an American Society of Anaesthesiologists (ASA) III score increased the risk of seroma 15.97 fold (P<0.001, 95% CI, 4.94 to 51.56), direct hernia type increased risk 7.1 fold (P<0.03, 95% CI, 1.204 to 42.422), hernia descending into scrotum increased risk 22.48 fold (P<0.001, 95% CI, 6.66 to 75.84) and closure of the peritoneal flap completely without leaving any defect increased the risk of seroma 8.67 fold (P<0.001, 95% CI, 3.254 to 23.115). CONCLUSIONS: The presence or leaving of small-diameter defects on the peritoneal flap may reduce seroma development without increasing the risk of complications. Prospective randomized studies are required to reach definitive conclusions.

Is the incision type important for the development of hernia in liver transplant patients?

OBJECTIVE: In this study, we aimed to investigate the rates and causes of incisional hernia that developed in the postoperative follow-up of patients who underwent liver transplantation. MATERIAL AND METHOD: The results of patients who underwent LT by using three different incisions at the Istanbul Yeni Yüzyil University Gaziosmanpasa Hospital organ transplant center between January 2015 and December 2019 were retrospectively analyzed. Patients were divided into Chevron (group-1), reverse T (group-2), and J incisions (group-3) and hernia development rates were examined. RESULTS: There was no significant difference in terms of incisional hernia in groups 1 and 2 according to the incision type (p = .723). Incisional hernia rate was significantly lower in the J incision group (p < .001). When the factors that increase the development of hernia in all LT patients were examined, it was seen that male gender (p = .021), high BMI rate (p = .003), postoperative bleeding (p = .018), and wound infection (p = .039) caused a significant increase in risk. CONCLUSION: The incision, which is made during liver transplant, is important for the development of hernia. The J incision has a low hernia development rate without causing access problems. Regardless of the incision, high BMI index, male gender, postoperative bleeding, and wound infection increase the development of incisional hernia in liver transplant patients.

When Should I Use an Additional Port at the Time of Three-Port Laparoscopic Cholecystectomy?

Objective: Today, it is recommended that the laparoscopic cholecystectomy (LC) is made with standard three ports. In this study, we aimed to determine the preoperative and intraoperative factors that require the use of an additional fourth port during three-port LC. Materials and Methods: All patients who started LC with three ports between January 1, 2018 and December 31, 2019 were included in the study. The patients were divided into two groups as those who underwent three-port LC and those who required additional ports. Independent parameters affecting the transition from three ports to four ports were analyzed using logistic regression analysis. The patients who underwent LC with three ports were included in Group 1 and the patients requiring an additional port were included in Group 2. Results: A total of 234 patients (139 women and 95 men) were included in the study. The average age of patients was 52.95 ± 16.26 (20-89) and body mass index is 28.64 ± 5.4 (15.73-48.89), respectively. Three ports were used in 148 patients (Group 1), and an additional fourth port was used in 42 patients (Group 2). Female gender, history of upper laparotomy, presence of acute infection findings, urgent surgery, and advanced age were observed to increase the use of additional ports. In multivariate analysis, it was shown that the presence of hepatic barrier (P < .001) and the presence of complete adhesion in the gallbladder (P < .001) significantly increased the use of additional trocars during LC. In addition, female gender was found to cause an increase of 6.62 times (P < .001). Conclusion: Many factors may require the use of additional ports during three-port LC. The use of an additional fourth port should not be avoided, especially in cases where hilum dissection is prevented due to liver origin, in female patients and in cases with complete adhesion to the gallbladder.

Surgical approach to recurrent secondary aortoenteric fistulas: A case report.

The increasing number of abdominal aortic grafts due to abdominal aortic aneurysms has caused secondary aortoenteric fistulas to be seen more frequently as a cause of gastrointestinal bleeding. High index of suspicion plays a significant role in the diagnosis in patients having clinical symptoms ranging from fecal occult blood to massive gastrointestinal bleeding, accompanied by hemorrhagic shock. A 65-year-old male patient developed two secondary aortoenteric fistulas consecutively. The first one was aortic graft-jejunal and the second one was aortic graft-duodenal in a short period. Secondary aortoenteric fistula developed after aortobifemoral bypass. The patient underwent graft revision and jejunal repair. He was reoperated three months later due to the newly developed aortic graft-duodenal fistula. The duodenal defect was closed, and an extra-anatomic aortoiliac bypass was performed to avoid graft-related enteric fistula. The patient was discharged uneventfully and was free from any complication at nine months after surgery.

[Fournier's gangrene: analysis of risk factors affecting the prognosis and cost of therapy in 18 cases]. / Fournier gangreni: 18 olgudaki prognoza etki eden risk faktörlerinin ve tedavi maliyetinin degerlendirilmesi.

BACKGROUND: Fournier's gangrene (FG) is a rapidly progressive, polymicrobial, synergistic necrotizing fasciitis, and the mortality rate is still high. We aimed to determine the risk factors affecting prognosis and treatment cost. METHODS: Eighteen patients operated for FG during 2003-2007 were investigated retrospectively. Surviving and exitus groups were compared regarding demographic data, etiological factors, laboratory findings, treatment modality, length of hospital stay, and treatment cost. RESULTS: Mean age was 54.5 years, and the female/male ratio was 6/12. Mortality was observed in 6 (33.3%) patients and was significantly high among females (66.6%) (p=0.035). Mean duration of complaint in the exitus group (9+/-3 days) was higher than in survivors (5+/-3 days) (p=0.018). The most frequent comorbid disease was diabetes (39.2%), the most frequent etiology was perianal abscess (55.6%) and the primary location of infection was anorectal region (61.1%). Hyponatremia was significantly high in surviving patients (p=0.039). Mean of FG severity point in the exitus group (6.83) was higher than in survivors (3.17) (p=0.011). The most frequently cultivated microorganism, Escherichia coli (66.6%), was significantly high in the exitus group (p=0.012). The mean number of debridements was 4.67. Fecal diversion was performed in 7 (38.8%) patients. Hospital stay in the surviving group (34.17 days) was higher than in the exitus group (10.50 days) (p=0.002). Treatment cost between groups was indifferent (p>0.05). CONCLUSION: Female gender, duration of complaint, FG severity point, and cultivated microorganism (E. Coli) were thought to affect mortality. FG is a disease that might cause extended hospital stay and high treatment cost.

The monitoring of progress in apoptosis of liver cells in bile duct-ligated rats.

BACKGROUND/AIMS: We aimed to determine the progress of lipid peroxidation and ultrastructural changes established in the rat liver after acute bile duct ligation. METHODS: Groups A1, B1, C1 and D1 were the controls of groups A2, B2, C2 and D2, which represented the 1st, 3rd, 5th and 8th days after bile duct ligation. Serum bilirubin and malondialdehyde, liver malondialdehyde and reduced glutathione levels, and inducible nitric oxide synthase expression were determined. Liver tissue was examined with light and electron microscopy. RESULTS: Serum bilirubin increased progressively. Serum and liver malondialdehyde and inducible nitric oxide synthase expression reached a peak level at day 3, reduced at the 5th day and continued at a constant rate. Reduced glutathione decreased progressively. Ductal proliferation increased progressively to a plateau at day 5. The marked electron microscopic changes were detected at day 3 (B2) and continued constantly. CONCLUSIONS: The first five days after acute bile duct ligation are the most critical.

Effects of sulfasalazine on lipid peroxidation and histologic liver damage in a rat model of obstructive jaundice and obstructive jaundice with lipopolysaccharide-induced sepsis.

BACKGROUND: Sulfasalazine, an inhibitor of cyclooxygenase, 5-lipoxygenase, and nuclear factor κB (NF-κB), has been found to alleviate oxidative damage, proinflammatory cytokine production, bile-duct proliferation, neutrophil infiltration, and fibrosis. Therefore, it may have a potential effect in attenuating lipid peroxidation and histologic liver damage in patients with biliary obstruction and biliary obstruction with sepsis. OBJECTIVE: The aim of this study was to investigate the effect of sulfasalazine on lipid peroxidation and histologic liver damage due to obstructive jaundice (OJ) and to OJ with lipopolysaccharide (LPS)-induced sepsis in an experimental model. METHODS: Male Wistar rats, weighing 150 to 220 g, were randomized into 6 groups: OJ; OJ + LPS; OJ + sulfasalazine; OJ + sulfasalazine + LPS (sulfasalazine administered before sepsis); OJ + LPS + sulfasalazine (sulfasalazine administered after sepsis); and sham. Liver malondialdehyde (MDA) and myeloperoxidase (MPO) activities were assessed to monitor lipid peroxidation and neutrophil infiltration in liver tissue. Histologic liver damage was evaluated with hematoxylin-eosin stained slides. Liver tissue NF-κB and caspase-3 expression were studied immunohistopathologically to evaluate lipid peroxidation, liver damage, and hepatocyte apoptosis. RESULTS: Forty-eight rats were evenly randomized into 6 groups of 8. MDA (P = 0.001), MPO (P = 0.001), NF-κB (P = 0.003), caspase-3 expression (P = 0.002), and liver injury scores (P = 0.002) increased significantly in the OJ group compared with the sham group. Compared with the OJ group, MDA (P = 0.030) and MPO levels (P = 0.001), and liver injury scores (P = 0.033) were decreased significantly in the OJ + sulfasalazine group. In the OJ + sulfasalazine + LPS and OJ + LPS + sulfasalazine groups, MDA (P = 0.008 and P = 0.023, respectively) and MPO (both, P = 0.001) were significantly decreased; however, liver NF-κB, caspase-3 expression, and liver injury scores were not significantly different compared with the OJ + LPS group. There was no significant difference between the OJ + LPS + sulfasalazine and OJ + sulfasalazine + LPS groups in regard to all end points when comparing the effects of sulfasalazine administered before or after sepsis. CONCLUSIONS: Sulfasalazine was associated with decreased neutrophil accumulation and lipid peroxidation in these rats with OJ. Administration of sulfasalazine before or after LPS-induced sepsis was associated with a reduction in lipid peroxidation and neutrophil accumulation; however, it did not attenuate histologic liver damage. There was no difference between the findings when sulfasalazine was administered before or after sepsis in OJ.

Liver tissue inducible nitric oxide synthase (iNOS) expression and lipid peroxidation in experimental hepatic ischemia reperfusion injury stimulated with lipopolysaccharide: the role of aminoguanidine.

BACKGROUND: Hepatic ischemia-reperfusion (HIR) is a severe condition that is seen after hepatic arterial injury and in hepatic grafts in living donor transplantation. HIR not only causes liver injury by lipid peroxidation, but also stimulates systemic and portal endotoxemia. Also, lipopolysaccharide (LPS) induces hepatic injury mediated by inducible nitric oxide synthase (iNOS). There is little knowledge on the role of specific iNOS inhibitors in prevention of HIR injury followed by LPS administration. The aim of this study on a LPS induced HIR model was to investigate the effect of aminoguanidine (AG) administration on hepatic tissue iNOS expression and lipid peroxidation when given before or after LPS. METHODS: Six groups were designed; A: Sham, B: HIR, C: HIR + AG, D: HIR + LPS, E: HIR + LPS + AG, F: HIR + AG + LPS. No substance was given to the rats in Group A and B. HIR injury was induced with vascular occlusion for 45 min and reperfusion for 45 min. Drugs were given intraperitoneally 10 min before reperfusion. Serum and tissue analysis for myeloperoxidase (MPO), and malondialdehyde (MDA), and tissue NA+/K+ adenosine 5'triphosphatases (ATPase) and tissue iNOS staining were performed. Permission for this study was obtained from the local Ethics Committee. RESULTS: The level of MPO, MDA, and iNOS staining scores in Group B were significantly higher than Group A and ATPase was lower in Group B (P < 0.05). Contrary to results in Group C, results of MPO, MDA, and iNOS staining scores of Group D was higher than Group B (P < 0.05); however, although iNOS in Group C was lower than Group B, the difference was not significant (P > 0.05). MPO and MDA levels of Groups E and F were significantly lower than Group D. Level of ATPase in Group F was significantly different from Groups D and E. iNOS scoring was low in Group F compared with Group D (P < 0.05). MDA, MPO, and iNOS levels of Group F was lower than Group E, and ATPase of Group F was higher than Group E (P < 0.05). CONCLUSIONS: The results of this study in a LPS induced HIR model showed that LPS after HIR aggravated HIR injury by increasing neutrophil activation and lipid peroxidation both in serum and liver tissue and iNOS in liver, and depleting energy in liver. AG, a selective iNOS inhibitor, ameliorated the negative effects of endotoxemia induced by LPS after HIR; however, energy depletion and iNOS expression in liver tissue were attenuated only when AG was administered prior to LPS. The findings of this study supported the hypothesis that LPS after HIR would aggravate HIR injury and AG would ameliorate this aggravated injury.

Laparoscopic removal of an incidental ectopic liver: short report of a case.

Ectopic liver is a rare clinical entity, which may be rarely of clinical importance. It is generally reported to be small in size and without a connection to the mother liver. A case of an incidental ectopic liver nodule that was connected with a vascular peduncle to the Couinad segment IVa of the liver has been reported. Microscopic examination revealed chronic inflammatory changes, which should be considered to be the result of intermittent circulatory disturbances.

The effects of exogenous l-carnitine on lipid peroxidation and tissue damage in an experimental warm hepatic ischemia-reperfusion injury model.

BACKGROUND: l-Carnitine is the essential endogenous factor for the transport of long-chain fatty acids from the cytoplasm to within the mitochondrion where the ß-oxidation process takes place. l-Carnitine is a superoxide scavenger and an antioxidant that possesses an anti-ischemic action and a stabilizing effect on cell membranes. It may be of help in liver ischemia reperfusion injury. RESULTS regarding the effects of l-carnitine on liver ischemia and reperfusion injury are few and conflicting. OBJECTIVE: The aim of this study was to investigate the efficacy of exogenous l-carnitine on lipid peroxidation and protecting liver at different stages of experimental total warm hepatic ischemia-reperfusion (TWHIR) procedure in rats. METHODS: This experimental study in healthy, weanling, male Wistar rats (weighing 180-200 g) was conducted at the Experimental Animal Research Laboratory of the Faculty of Medicine of Mersin University, Mersin, Turkey. Rats were randomly divided into 5 groups: (A) Control group; (B) TWHIR procedure only; (C) l-carnitine administered 2 hours before the TWHIR procedure; (D) l-carnitine administered just before the TWHIR procedure; and (E) l-carnitine administered after total warm hepatic ischemia but just before the reperfusion procedure. Total warm hepatic ischemia (via the Pringle maneuver) and reperfusion were performed for 45 and 30 minutes, respectively. l-Carnitine (200 mg/kg) was administered intravenously. At the end of each procedure a blood sample was drawn and total hepatectomy was performed following reperfusion. Malondialdehyde (MDA) and myeloperoxidase (MPO) levels of both plasma and liver tissue, total antioxidant capacity (TAOC), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in plasma, and histopathologic examination were analyzed to assess lipid peroxidation and damage in liver tissue. RESULTS: Thirty-four rats (mean [SD]age, 59.26 [1.2]days; mean [SD] weight, 194.1 [5.1] g) were used in the study. There was a significant difference observed between groups A (n = 5) and B (n = 5) for all evaluation parameters. The TWHIR procedure performed in group B was associated with significant increases versus baseline in ALT, AST, MDA, and MPO in plasma, and MDA and MPO in liver tissue, but a significant decrease of TAOC in plasma. ALT, AST, serum and liver MDA, and MPO levels of group B were significantly higher than all groups administered l-carnitine. l-Carnitine administration between total warm hepatic ischemia and reperfusion was associated with a significant attenuation in all parameters. The liver MDA levels of groups C (n = 8) and D (n = 8) were significantly lower than that of group E (n = 8) (mean [SD]: C, 16.53 [3.32] and D, 18.28 [1.67] vs E, 23.05 [3.52]; P = 0.001 and P = 0.016, respectively). The mean (SD) liver MPO level of group C (1.09 [0.16]) was significantly lower than that of groups D (2.12 [0.25]) and E (2.11 [0.28]) (both, P = 0.001). The TAOC of group B (0.77 [0.12]) was significantly lower than that of groups C (1.34 [0.19]) and D (1.08 [0.20]) (P = 0.001 and P = 0.015, respectively). The TAOC of group C was significantly higher than that of the other l-carnitine groups (E, 0.94 [0.13]) (P = 0.023 vs group D; and P = 0.001 vs group E). Histopathologic scores of groups A, C, and E were significantly lower than that of group B, but the difference between groups B and D was not statistically significant. CONCLUSIONS: In this experimental study, administration of exogenous l-carnitine was associated with significantly decreased lipid peroxidation in plasma and liver tissue when administered prior to a TWHIR procedure. In addition, l-carnitine seemed to be more effective with regard to decreasing lipid peroxidation in liver tissue when administered before warm hepatic ischemia. l-Carnitine was associated with significantly decreased leukocyte sequestration in plasma and liver tissue. A significant increase in TAOC was associated with l-carnitine administered prior to ischemia. These observations suggest that l-carnitine might have a protective effect against ischemia-reperfusion injury in rat liver tissue.

Effect of N-acetylcysteine on blood and tissue lipid peroxidation in lipopolysaccharide-induced obstructive jaundice.

In obstructive jaundice, free radical production is increased and antioxidative activity is reduced. N-Acetylcysteine (NAC) has a beneficial effect with anti-inflammatory and antioxidant activity, acting as a free radical scavenger. NAC inhibits inducible nitric oxide synthase, suppresses cytokine expression/release, and inhibits adhesion molecule expression and nuclear factor kappa B. The aim of this study was to investigate the effects of NAC on liver/renal tissue and serum lipid peroxidation in lipopolysaccharide (LPS)-induced obstructive jaundice. We randomized 60 rats into 6 groups: group 1, Sham; group 2, obstructive jaundice (OJ) induced after bile-duct ligation; group 3, OJ + NAC (100 mg kg- 1 subcutaneously); group 4, OJ + LPS (10 mg kg-1); group 5, OJ + NAC + LPS; and group 6, OJ + LPS + NAC. For each group, the biochemical markers of lipid peroxidation and the antioxidant products were measured in serum and liver/renal tissue after sacrifice. Almost all lipid peroxidation products levels were increased and antioxidant products levels were decreased in groups who received LPS (groups 4, 5, and 6), but the effect was less remarkable when NAC was administered before LPS (group 5). The same trend was seen for groups with OJ +/- LPS who did not received NAC or received it after induced toxemia (groups 2, 4, and 6) as compared to groups 1 and 3. Moreover, in the case of OJ + LPS, rats treated with NAC before LPS (group 5) had lower lipid peroxidation products levels and higher antioxidant products levels as compared to those who did not received NAC (group 4). This phenomenon was not reproducible with NAC administered after LPS (group 6). Thus, results of this study showed that NAC prevents the deleterious effects of LPS in obstructive jaundice by reducing lipid peroxidation in serum and liver/renal tissue if administered before LPS. Nonetheless, NAC failed to prevent the lipid peroxidation in the case of established endotoxemia in obstructive jaundice.

The effect of aminoguanidine on blood and tissue lipid peroxidation in jaundiced rats with endotoxemia induced with LPS.

Obstructive jaundice (OJ) is a severe condition that leads to several complications. One of the important problems in OJ is the increased incidence of endotoxemia, which is the result of bacterial translocation (BT) and defective host immune response. Lipid peroxidation (LP) is an important problem in OJ and sepsis in which nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity are increased and antioxidative activity is decreased. Formation of peroxynitrite (ONOO(-)) anion leads to cellular damage and apoptosis. In this experimental study, we explore the effect of specific iNOS inhibitor aminoguanidine (AG) on blood and tissue (liver and renal) LP and iNOS levels in jaundiced rats with endotoxemia induced with lipopolysaccharide (LPS). Rats were randomized into six groups; group A, sham; group B, obstructive jaundice (OJ); group C, OJ + LPS; group D, OJ + AG; group E, OJ + LPS + AG; group F, OJ + AG + LPS. Serum malondialdehyde (MDA) and serum myeloperoxidase (MPO) activity and liver and renal tissue MDA, MPO, and Na(+)/K(+)-ATPase activity levels were detected in biochemical methods. Liver and renal tissue iNOS levels were examined immunohistopathologically. Serum and tissue MDA and MPO levels and tissue iNOS expression were increased significantly in groups B, C, and E, while tissue ATPase levels were decreased significantly in the same groups. In the group treated with AG (group D), serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. In group F, if AG was administrated before LPS, we observed that serum and tissue MDA and MPO levels and tissue iNOS expression were decreased while tissue ATPase levels were increased significantly. Thus, our study showed that AG had a protective effect when it was administrated before LPS, but it failed to prevent tissue iNOS expression and LP if there was established endotoxemia in OJ.

Intestinal perforation in Wegener's granulomatosis: a case report.

Wegener's granulomatosis is a disease characterized by a necrotizing vasculitis and granulomatous inflammation. The localized form involves the upper and/or lower respiratory tracts while in the common generalized form there is a widespread necrotizing vasculitis and renal involvement. Although gastrointestinal involvement which has been detected at necropsy in 24% of the cases is an uncommon finding, it might cause severe complications. We report a patient with clinical Wegener's granulomatosis who subsequently developed gastrointestinal perforation. Gastrointestinal perforation was treated with surgical resection and the patient survived under the treatment of cyclophosphamide and prednisolone with no further gastrointestinal complications. The present case indicates that the gastrointestinal complications might be considered in natural history of Wegener's granulomatosis.

The effect of N-acetylcysteine on pulmonary lipid peroxidation and tissue damage.

BACKGROUND: We aimed to investigate the effect of N-acetylcysteine (NAC) on pulmonary lipid peroxidation and tissue damage in experimental obstructive jaundice (OJ) stimulated by lipopolysaccharide (LPS) in this study. MATERIALS AND METHODS: We randomized 40 rats into five groups. Group A: Sham (n = 8); group B: OJ (n = 8); group C: OJ + lipopolysaccharide (LPS; n = 8); group D: OJ + NAC + LPS (n = 8); group E: OJ + LPS + NAC (n = 8). OJ was performed by common bile duct ligation and division in all groups except the sham group. At the fifth day, the rats were jaundiced. At the fifth day of OJ, LPS was injected 10 mg/kg intraperitoneally to the rats and at the tenth day, the rats were sacrificed in group C. In group D; at the fifth day of OJ, NAC was started 100 mg/kg subcutaneously and the same dose NAC injection repeated every day for 5 days. At the tenth day of OJ, LPS was injected 10 mg/kg intraperitoneally to the rats and then after 6 h they were sacrificed. In group E; 10 mg/kg LPS was administered intraperitoneally at fifth day of OJ and after then NAC was started 100 mg/kg subcutaneously and the same dose NAC injection repeated every day for 5 days and at the tenth day, the rats were sacrificed. Tissue samples were harvested through a midline incision, and lungs were resected and examined histopathologically and immunohistochemically for tissue damage scoring. The blood was taken by cardiac puncture and malondialdehyde (MDA), myeloperoxidase (MPO), and levels of total antioxidant status were detected with biochemical methods to evaluate lung tissue damage. RESULTS: Increase in lung and serum MDA and MPO levels, as well as decrease in total antioxidant status, were observed in groups B and C when compared with the sham group (P = 0.0001, for each comparison). Furthermore, the lung tissue damage was observed in the same groups by histopathological examination when compared with sham group. There was significant decrease at serum and lung MPO and MDA levels after the NAC application in groups D and E, when compared with group C (P = 0.0001, for each comparison). Antioxidant status in groups D and E were increased in the presence of NAC (P = 0.0001, for each comparison). Lung histology was prevented relatively in group D when compared with groups B and C. CONCLUSION: Results of the study indicate that NAC has protective effect on pulmonary lipid peroxidation and tissue damage before and after LPS administration.

[A case of superior mesenteric artery syndrome following head trauma]. / Kafa travmasi geçiren bir hastada süperior mezenterik arter sendromu.

A twenty-four-year-old male patient developed a high level gastrointestinal obstruction during hospitalization in intensive care unit following a head trauma. He suffered from vomiting and weight loss and was unable to tolerate nasoenteral feeding. Barium radiographs revealed obstruction in the third portion of the duodenum. Upon failure of conservative treatment, laparotomy was performed, which showed compression and obstruction of the third portion of the duodenum by the superior mesenteric artery. A side-to-side duodenojejunostomy performed yielded complete relief of compression symptoms. The patient was symptomless in the sixth postoperative year. Although primary treatment of superior mesenteric artery syndrome is conservative, surgical treatment should be considered in unresponsive patients.

The effect of N-acetylcysteine (NAC) on liver and renal tissue inducible nitric oxide synthase (iNOS) and tissue lipid peroxidation in obstructive jaundice stimulated by lipopolysaccharide (LPS).

Morbidity and mortality rates are very high in obstructive jaundice when it is associated with sepsis and multiple organ failure. Nitric oxide (NO) formation and increased expression of inducible nitric oxide synthase (iNOS) also take place in obstructive jaundice (OJ). N-Acetylcysteine (NAC) has a beneficial effect by demonstrating anti-inflammatory activity such as inhibits cytokine expression/release, inhibiting the adhesion molecule expression and inhibiting nuclear factor kappa B (NFkappaB). The aim of this study was to investigate the effects of NAC on liver and renal tissue iNOS, and liver tissue lipid peroxidation in lipopolysaccharide (LPS) induced obstructive jaundice. We randomized 48 rats into six groups. Group A: Sham group; group B: OJ group; group C: OJ+NAC; group D: OJ+LPS (Escherichia coli LPS serotype L-2630, 100mg, Sigma) group E: OJ+NAC+LPS; group F: OJ+LPS+NAC. NAC was started subcutaneously 100mg/kg. LPS was injected intraperitoneally and then at the tenth day we sacrificed the rats. Liver malondialdehyde (MDA) increased and liver ATPase decreased in groups B-D when compared to group A. After the administration of NAC (groups C-E), liver MDA levels decreased, tissue ATPase levels increased as compared to other groups. The liver and renal tissue iNOS expression was increased in groups B, D, and F. After the administration of NAC (groups C-E) the liver and renal tissue iNOS expression were decreased. Our results indicated that NAC prevented the deleterious effects of LPS in OJ by reducing iNOS expression via lipid peroxidation in liver and renal tissue; if it was administrated before LPS. But NAC failed to prevent the iNOS expression and lipid peroxidation if there was established endotoxemia in OJ.

The effect of preoperative intravenous use of tenoxicam: a prospective, double-blind, placebo-controlled study.

In this study, we aimed to investigate the postoperative pain relief effect of preoperative tenoxicam usage in patients who undergo elective laparoscopic cholecystectomy or groin hernia repair. Eighty patients undergoing laparoscopic cholecystectomy or groin hernia repair procedures were randomized to receive either physiologic serum at 100 mL (group I, n = 40) or 20 mg iv tenoxicam (group II, n = 40) immediately before induction. Postoperative analgesic requirement, peroperative side effects and complications of drugs, operating time, post-operative mobilization time and pain score, hospitalization time, and patient pleasure were recorded. Postoperative pain was assessed by the visual analogue scale (VAS) on the recovery unit (RU), at 4, 8, and 24 h and every day at the same times in the morning. The RU median VAS score was also not different when Group 1 was compared with Group 2 (p = .97). However, the postoperative 4-h and 8-h median VAS score was significantly less (p = .01 and p = .03, respectively); first postoperative mobilization time was earlier in group 2 (p = .32). The median pain score and intramuscular analgesic requirement of patients were also reduced in Group 2 in postoperative day 1 (p = .015). The median duration of intramuscular analgesic requirement and total amount of intramuscular analgesic used in patients were also significantly less in Group 2 (p = .0001 and p = .0001, respectively). Thus, this study showed that preoperative use of iv tenoxicam is safe, simple, and effective for postoperative pain relief after laparoscopic cholecystectomy or inguinal hernia repair.

Effect of ornithine on the ileal histology, nitric oxide production and lipid peroxidation in LPS-induced endotoxemia.

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.

The effect of PARS inhibition on ileal histopathology, apoptosis and lipid peroxidation in LPS-induced obstructive jaundice.

In our experimental study, we investigated the protective effect of 3-aminobenzamide (3-AB), the poly (ADP-ribose) synthetase (PARS inhibitor), on the ileal histopathology and the apoptosis in lipopolysaccharide (LPS)-induced inflammation in rats with obstructive jaundice (OJ). We randomized 40 rats into five groups. Group 1: sham group; Group 2: OJ group; Group 3: OJ+LPS; Group 4: OJ+3-AB+LPS; Group 5: OJ+LPS+3-AB. At the fifth day; the rats were jaundiced. In Group 3; 10 mg kg(-1) LPS was injected intraperitoneally at the fifth day and then after 6h the rats were sacrificed. In Group 4; 10 mg kg(-1) 3-AB was administrated intraperitoneally at the fifth day and repeated daily for 3 days and at the eighth day, 10 mg kg(-1) LPS was injected intraperitoneally. In Group 5, 10 mg kg(-1) LPS was injected intraperitoneally at the fifth day and after 6h 10 mg kg(-1) 3-AB was administrated intraperitoneally and repeated daily for 3 days. At the eighth day, rats were sacrificed. Blood samples were taken for detection of serum MDA levels. Ileum samples were taken after relaparotomy for histopathological examination to evaluate the endotoxin-related intestinal injury and Caspase-3 apoptosis and for detection of tissue MDA and ATPase activities. There was marked destruction of villous and crypt epithelial cells and extensive apoptosis in Groups 3 and 5 in histopathological examination. In Group 4, the scores of intestinal mucosal damage and apoptotic cells were reduced significantly (P<0.05). On the other hand, the scores of intestinal mucosal damage and apoptotic cells were not improved in Group 5. After the administration of 3-AB (Group 4), serum and ileal MDA levels decreased, ileal ATPase increased as compared to Groups 1 and 2. Our study showed that 3-AB prevented the mucosal damage and apoptotic loss of intestinal epithelial cells significantly if it was administrated before LPS. However, 3-AB failed to prevent the mucosal damage and apoptotic loss of intestinal epithelial cells significantly if there was established endotoxemia in OJ.