Ali Nayci

Intestinal ischemic preconditioning protects the intestine and reduces bacterial translocation.

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.

Dexamethasone Down-Regulates Endothelial Expression of Intercellular Adhesion Molecule and Impairs the Healing of Bowel Anastomoses

OBJECTIVE To find out the role of endothelial expression of intercellular adhesion molecule-1 (ICAM-1) in the healing of intestinal anastomoses in rats, and to establish the effects of peroperative treatment with corticosteroids. DESIGN Experimental animal study. SETTING University hospital, Turkey. MATERIAL 78 Male Wistar rats. INTERVENTIONS Rats were divided into four groups: Group I, colonic anastomosis only (=18); Group II, colonic anastomosis plus caecal ligation and puncture (=18); Group III, colonic anastomosis plus dexamethasone (=18); and Group IV, colonic anastomosis, plus caecal ligation and puncture, plus dexamethasone (=18). Six animals served as the sham group. The animals underwent bowel transsection and primary anastomosis Infection was produced by caecal ligation and puncture Preoperatively, dexamethasone was given intramuscularly in a dose of 2 mg/kg/day. MAIN OUTCOME MEASURES After 1, 3 and 5 days, anastomotic healing and endothelial expression of ICAM-1 were measured microscopically. RESULTS Anastomotic healing was significantly impaired in dexamethasone-treated animals, and endothelial expression of ICAM-1 was reduced. Endothelial expression of ICAM-1 was no higher in the infected group than in controls. Maximum expression of ICAM-1 on endothelial cells was seen on the first day in each group, and declined on the following days, although the sebsequent reduction in expression was not significant. CONCLUSION Dexamethasone down-regulated expression of ICAM-1, which is important in migration of leucocytes from the circulation to the wound site, and significantly impaired the healing of intestinal anastomoses in rats.

THE EFFECTS OF DEXAMETHASONE ON LIPID PEROXIDATION AND NITRIC OXIDE LEVELS ON THE HEALING OF TRACHEAL ANASTOMOSES: AN EXPERIMENTAL STUDY IN RATS

Corticosteroids are shown to have deleterious effects on wound healing for various tissues. Arginine metabolism and nitric oxide (NO) synthesis play an important role in many aspects of inflammation and wound healing. The study was designed to evaluate the relationship of dexamethasone impaired healing of tracheal anastomoses to NO metabolism and lipid peroxidation. Forty-two adult Wistar rats were randomly divided into five groups. The animals underwent tracheal transection and primary anastomoses. The groups were assigned as follows: Group I (GI) (sham, N = 6); Group II (GII) (control, N = 6); Group III (GIII), dexamethasone, 0.1 mg kg(-1) per day, intramuscularly for a week (N = 10); Group IV (GIV), dexamethasone, 1 mg kg(-1) per day, intramuscularly for a week (N = 10); Group V (GV), dexamethasone, 6 mg kg(-1) intramuscularly as a single dose (N = 10). After 7 days, bursting pressure was used to evaluate anastomotic healing. Serum nitrite/nitrate and malondialdehyde (MDA) levels were measured as an index of NO synthesis and lipid peroxidation, respectively. The bursting pressure significantly decreased in GIII and GIV when compared to the control group. The difference between GIII and GIV was also statistically significant. Nitrite/nitrate and MDA levels of GIII were found to be significantly higher than the control group. Also, the difference was found to be statistically significant between GIII and GIV in regard to nitrite/nitrate levels. The present study demonstrates that daily administration of dexamethasone for a week inhibits NO synthesis in a dose-dependent manner on tracheal anastomotic healing. Besides the generally accepted evaluation parameters including bursting pressure and hydoxyproline content; NO and MDA levels may be helpful in the assessment of wound healing especially for the investigation of impairment mechanism.

Ileal atresia associated with a congenital vascular band anomaly: observations on pathogenesis

We report the case of a newborn, who developed intestinal obstruction soon after birth. Exploratory laparotomy revealed a congenital vascular band anomaly extending from the antimesenteric border of the terminal ileum to the gallbladder in association with ileal atresia. Surgical intervention was performed for correction of the disorder. A review of the embryology and congenital vascular bands is presented together with discussion as to possible etiopathogenesis leading to small bowel atresia.

The effects of corticosteroids and vitamin A on the healing of tracheal anastomoses

OBJECTIVE This study investigates the deleterious effects of corticosteroids on tracheal anastomotic healing and the ability of vitamin A to reverse these effects in a rat model. METHODS Forty-two adult Wistar rats were randomly divided into five groups. The animals underwent tracheal transection and primary anastomoses. The groups were assigned as follows: Group I, sham (N=6); Group II, control (N=6); Group III, dexamethasone, 0.1 mg/kg/day intramuscularly (N=10); Group IV, dexamethasone 0.1 mg/kg/day intramuscularly+vitamin A 10000 IU/kg/day by gavages (N=10); and Group V, vitamin A 10000 IU/kg/day by gavages for a week (N=10). After 7 days, anastomotic healing was assessed by measurement of bursting pressure, hydroxyproline content and subsequent histological grading using the modified Ehrlich/Hunt scale. RESULTS Bursting pressures and hydroxyproline contents were as follows: Group I: 977+/-8 mmHg and 11.80+/-0.3 microg/mg (mean+/-standard error of the mean); Group II: 890+/-55 mmHg and 9.93+/-0.6 microg/mg; Group III: 555+/-26 mmHg and 11.90+/-1.3 microg/mg; Group IV: 873+/-73 mmHg and 10.24+/-2.2 microg/mg; Group V: 905+/-45 mmHg and 7.51+/-0.8 microg/mg, respectively. Bursting pressure of Group III was found to be significantly lower when compared to other groups (P<0.0001). However, statistical significance was not found among the study groups for the hydroxyproline content. Except for inflammatory cell infiltration, histological parameters including epithelial regeneration, fibroblast proliferation, collagen content, and angiogenesis demonstrated significant differences among the groups. CONCLUSION The present study demonstrates that dexamethasone significantly impairs the healing of tracheal anastomoses in rats and postoperative administration of vitamin A appreciably reverses this inhibitory effect. Patients receiving corticosteroids may benefit from vitamin A when undergoing prolonged intubation and laryngotracheal reconstruction.

Platelet-activating factor antagonist (ABT-491) decreases neuronal apoptosis in neonatal rat model of hypoxic ischemic brain injury

Hypoxic ischemic brain injury (HIBI) is a common cause of neonatal mortality and morbidity. To date, no study has investigated the role of platelet-activating factor (PAF) antagonists on neuronal apoptosis in neonatal rat model of HIBI. In the present study, we evaluated the effect of a highly potent and selective PAF antagonist (ABT-491) on neuronal apoptosis in neonatal rat model of HIBI. Seven-day-old Wistar rat pups were subjected to right common carotid artery ligation and hypoxia (92% nitrogen and 8% oxygen) for 2 h. They were treated with ABT-491 or saline either immediately before or after hypoxia. In sham group animals, neither ligation, nor hypoxia was performed. Neuronal apoptosis was evaluated by the terminal-transferase mediated dUTP biotin nick-end-labeling (TUNEL) and caspase-3 staining methods. Administration of ABT-491 either before or after hypoxia resulted in significant reduction of the numbers of apoptotic cells in both hemispheres, when compared to saline treatment group. The numbers of apoptotic cells in right hemispheres in all groups were significantly higher than that in the left hemispheres. These results suggested that ABT-491, a highly potent and selective PAF antagonist, administration either before or after hypoxia reduces apoptosis and we propose that ABT-491 may be a novel approach in the treatment of HIBI.

Effects of trapidil on the healing of colonic anastomoses in an experimental rat model.

Background:  Trapidil has various properties including vasodilatation, inhibition of lipid peroxidation and platelet aggregation as well as, and reduction of, the inflammatory response to injury. The aim of the present study was to investigate the effects of trapidil on dexamethasone‐impaired colonic anastomotic healing in an experimental rat model.

Relationships among vesicoureteric reflux, urinary tract infection and renal injury in children with non-neurogenic lower urinary tract dysfunction.

OBJECTIVE To determine the relationship between vesicoureteric reflux (VUR), urinary tract infection (UTI), renal damage and the pattern of non-neurogenic lower urinary tract dysfunction (LUTD), and to reveal the possible risk factors for renal damage in children with LUTD. METHODS For the years 2004-2010, demographic, clinical, laboratory and urodynamic study reports of children with LUTD were retrospectively reviewed. RESULTS Of 96 patients, there were diagnosed 70 with overactive bladder (OAB), 8 pure dysfunctional voiding (DV) and 18 OAB plus DV. The rate of VUR, UTI and renal damage in patients with OAB plus DV and pure DV was higher than in patients with OAB alone. VUR was significantly higher among the patients who had UTI. Renal scarring was detected in 25 patients, of whom 78% had OAB plus DV and 75% DV. The presence of VUR was associated with a significant increase in the rate of renal damage, and dilating reflux caused significantly greater damage compared to non-dilating reflux. CONCLUSION OAB plus DV and DV are major risk factors for VUR, UTI and renal damage. The presence of VUR in children with LUTD plays an important role with regard to UTI and renal damage, with dilating VUR a major risk factor associated with renal damage.

Rigid bronchoscopy induces bacterial translocation: an experimental study in rats

Bronchoscopy has the potential to propagate infections. Bacterial translocation was hypothesised to be the cause of infections observed following bronchoscopy and this study was designed to assess the risk of bacterial translocation following rigid bronchoscopy in rats. A total of 30 rats were evaluated. The study group (n=15) underwent rigid bronchoscopy. Arterial blood gas analysis was performed in all rats. Blood and tissue cultures from the ileum, caecum, mesenteric lymph nodes, liver, spleen, mediastinal lymph nodes and lung were obtained 24 h following bronchoscopy. Bacterial translocation to the mesenteric lymph nodes was found in seven of 15 rats (46.7%) that underwent bronchoscopy, compared with none of the controls. Of the seven positives, three rats (42.8%) also demonstrated other organ involvement, such as the liver and spleen. Escherichia coli, Salmonella typhymirium, S. enteritidis and Pseudomonas spp. were found as translocating bacteria. In the study group, pH and arterial oxygen tension were significantly lower and arterial carbon dioxide tension was higher, compared with controls. This study shows that rigid bronchoscopy may induce bacterial translocation in rats. Further investigations aimed at understanding the clinical consequences of this phenomenon are warranted.

N-acetylcysteine protects the rats against phrenic nerve dysfunction in sepsis.

This study investigates the association of oxidative stress with the function of the phrenic nerve and inquires whether N-acetylcysteine (NAC) may counteract the possible detrimental effects. Thirty rats were divided into three groups: sham, cecal ligation and puncture (CLP), and CLP plus NAC treatment. Sepsis was produced by the CLP procedure. NAC was administered at 70 mg/day for 7 days. Electrophysiology was evaluated by the needle electromyography of the diaphragm and phrenic nerve conduction study. Oxidative stress was evaluated by malondialdehyde (MDA), nitrite/nitrate (NN), and reduced-glutathione (ReGSH) levels and myeloperoxidase (MPO) and catalase (CAT) activities in the phrenic nerve. In the CLP group, ReGSH and CAT were decreased (P = 0.0001, P = 0.07, respectively); and MDA, MPO, and NN were increased (P = 0.02, P = 0.0001, P = 0.043, respectively), compared with the sham group. NAC administration increased the ReGSH (P = 0.036) and decreased the MDA, MPO, and NN (P = 0.008, P = 0.01, P = 0.032, respectively), compared with the CLP group. In the CLP group, electrophysiology revealed reductions in the number of motor unit action potentials (P = 0.0001) and prolongations in the latency of the compound nerve action potential (P = 0.0001), indicating phrenic nerve neuropathy. NAC administration significantly ameliorated these electrophysiological alterations (P = 0.011, P = 0.0001, respectively), compared with the CLP group. The present results showed that intraabdominal sepsis is closely associated with phrenic nerve neuropathy. In addition, NAC administration protects the rats against the detrimental events of sepsis.