Enteral nutrition affects nitric oxide production in peripheral blood and liver after a postoperative lipopolysaccharide-induced endotoxemia in rats.

OBJECTIVES: Sepsis is a common complication in the early postoperative period, leading to the augmentation of oxidative and nitrosative stresses. The present study investigated the role of enteral nutrition on nitric oxide (NO) production after a lipopolysaccharide (LPS)-induced endotoxemia as an index of nitrosative stress. METHODS: Fifty rats were subjected to midline laparotomy and feeding gastrostomy. Ten rats served as controls after recovering from operative stress. The remaining rats received, through gastrostomy, enteral nutrition or placebo feeding for 24 h, after which they were injected intraperitoneally with LPS or equal volume of saline. Two hours later blood and liver tissue were collected. NO production was quantified in serum samples and homogenates of liver tissue by a modification of Griess's reaction. NO synthase (NOS) mRNA expression was examined in homogenate of liver tissue by reverse transcription-polymerase chain reaction. RESULTS: The operation significantly increased basal NO production in rat serum. LPS induced a further significant increase of NO levels. Enteral feeding of rats significantly decreased NO levels in both groups. In contrast, enteral nutrition was found to increase significantly NO levels in liver homogenates from rats treated with LPS. A constitutive endothelial NOS mRNA expression was found in liver tissue, whereas LPS administration induced inducible NOS mRNA expression in liver tissue regardless of enteral feeding. CONCLUSION: These findings indicate that early enteral feeding leads to a reduction in circulating NO levels induced by operation and endotoxemia, but increases hepatic NO levels in endotoxemia probably by the effect of LPS-induced inducible NOS on the increased L-arginine uptake.

Endoprosthesis implantation at the pharyngo-esophageal level: problems, limitations and challenges.

AIM: To present our experience with endoscopic placement of an esophageal endoprosthesis in 19 patients. METHODS: A retrospective evaluation was made for the use of 19 stents positioned at the level of the cervical esophagus: 11 for malignant tumours (7 causing obstruction, 4 complicated by an esophago -tracheal or -cutaneous fistula), and 8 for an acquired benign tracheo-esophageal fistula due to prolonged intubation. The covered Ultraflex stent was used in all cases except two. These two patients had an esophagocutaneous fistula following laryngectomy and a Flamingo Wall stent was used. RESULTS: Stent implantation was technically successful in all patients. Dysphagia score was improved from 3 to 2 in stenosis patients, while sealing of the fistula was achieved in all cases. The median hospital stay was 3 d for malignant tumour patients and 13.5 d for esophagocutaneous fistula patients. One Ultraflex stent and two Flamingo Wall stents were easily removed 33 d and 3 months respectively after implantation when the fistulas had totally occluded. CONCLUSION: Endoprosthesis implantation for malignancy and/or fistula of malignant or benign origin at the level of the cervical esophagus is an easy, well tolerated, safe and effective procedure with no complications or mortality.

Hepatic microcirculation after continuous 7-day elevated intra-abdominal pressure in cirrhotic rats.

It is well known that IAP elevation, even at the level of 10mmHg used for laparoscopic surgery leads to an increase in portal pressure and decrease in portal blood flow. Since hepatic hemodynamics are already disturbed in cirrhotics, we decided to investigate the possible role of chronically elevated intra-abdominal pressure thus simulating ascites under tension-in liver perfusion and function in cirrhotic portal hypertensive rats. Four groups of 10 rats each were studied, including two control and two CCl(4)(-) induced cirrhotic groups. These were subdivided into normal and increased IAP. Elevation and maintenance of increased IAP to 20mmHg for 7 consecutive days was achieved by means of an intraperitonially placed balloon filled with water. Liver microcirculation was assessed by means of laser-Doppler technique, while venous blood samples were obtained for determination of the biochemical parameters of liver function. Cirrhotic rats showed a significant decrease in liver microcirculation in relation to controls (15.7+/-2.5 versus 23.2+/-2.2, p=0.001). Elevation of IAP led to a significant decrease (p=0.001) of liver microcirculation in both groups, i.e. from 15.7+/-2.5 to 12.7+/-1.7 units of flow in cirrhotics and from 23.2+/-2.2 to 15.9+/-2.6 units of flow in control rats. Alkaline phosphatase, alanine aminotransferase and bilirubin concentrations were found increased in cirrhotics in comparison to controls (p=0.05). IAP elevation resulted in a further impairment of liver function, but the differences, were not statistically significant. In conclusion, chronically elevated IAP in cirrhotic rats is associated with a significant impairment of the already decreased hepatic blood flow due to liver cirrhosis. Thus, the possible consequences of decreased liver perfusion must be taken under consideration in any case of severe cirrhosis presented with ascites under tension.

Oxidative stress due to anesthesia and surgical trauma: importance of early enteral nutrition.

Anesthesia and surgical trauma are considered major oxidative and nitrosative stress effectors resulting in the development of SIRS. In this study we evaluated the usefulness of early enteral nutrition after surgical trauma. Sixty male Wistar rats were subjected to midline laparotomy and feeding-gastrostomy. Twenty of these rats served as controls after recovering from the operation stress. The remaining rats received, through gastrostomy, enteral nutrition or placebo-feeding for 24 h. Oxidative stress markers and CC chemokine production were evaluated in rat serum and liver tissue. The operation itself was found to increase nitric oxide (NO) and malondialdehyde (MDA) and to decrease superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), as well as liver tissue energy charge (EC) in relation to controls. The rats receiving enteral feeding exhibited statistically significantly lower levels of NO and MDA, and higher levels of SOD, GSH-Px, and liver EC, in relation to placebo feeding rats. The operation significantly increased the chemokines monocyte chemoattractant protein (MCP)-1 and regulated upon activation, normal T-cell expressed, and secreted (RANTES) in rat serum, while enteral nutrition caused a further significant increase in chemokine levels in serum. mRNA chemokine expression in liver was increased in a similar pattern. These findings indicate that early enteral feeding might play an important role after surgery ameliorating oxidative stress, affecting positively the hepatic EC and regulating, via chemokine production, cell trafficking, and healing process.

Retroperitoneal compartment pressure elevation impairs pancreatic tissue blood flow.

OBJECTIVES: To investigate whether the increase of the retroperitoneal compartment pressure, as in the case of peripancreatic fluid accumulation in severe acute pancreatitis, simulated by infusing a colloid fluid into the retroperitoneum, has any effect on pancreatic tissue blood flow. METHODS: Six male anesthetized swine were subjected to a transcutaneous placement of catheters into the retroperitoneal space. Through these catheters, a colloid solution was infused, under continuous retroperitoneal pressure monitoring, to achieve a pressure up to 20 mm Hg. Pancreatic tissue blood flow was assessed by colored microsphere injection technique, and pancreatic interstitial pressure was measured by means of a commercially available pressure monitor system before and after the distension of the retroperitoneal space, allowing the appropriate time for the animals to be stabilized from any intervention. RESULTS: The increase in the retroperitoneal compartment pressure was found to significantly increase pancreatic interstitial pressure (from 8 +/- 1 to 20 +/- 2.4 mm Hg, P = 0.001) as well as reduce pancreatic tissue blood flow (from 1.75 +/- 0.4 to 0.56 +/- 0.12 mL . min . g, P = 0.002). CONCLUSIONS: The increase of retroperitoneal pressure leads to an impairment of pancreatic tissue blood flow in the healthy pancreas. Although these findings support the hypothesis that peripancreatic fluid collection during the course of acute pancreatitis could contribute or augment pancreatic tissue ischemia, further assessment is necessary.

Benefits of a synbiotic formula (Synbiotic 2000Forte) in critically Ill trauma patients: early results of a randomized controlled trial.

BACKGROUND: Since probiotics are considered to exert beneficial health effects by enhancing the host's immune response, we investigated the benefits of a synbiotics treatment on the rate of infections, systemic inflammatory response syndrome (SIRS), severe sepsis, and mortality in critically ill, mechanically ventilated, multiple trauma patients. Length of stay in the intensive care unit (ICU) and number of days under mechanical ventilation were also evaluated. METHOD: Sixty-five patients were randomized to receive once daily for 15 days a synbiotic formula (Synbiotic 2000Forte, Medipharm, Sweden) or maltodextrin as placebo. The synbiotic preparation consisted of a combination of four probiotics (10(11) CFU each): Pediococcus pentosaceus 5-33:3, Leuconostoc mesenteroides 32-77:1, L. paracasei ssp. paracasei 19; and L. plantarum 2,362; and inulin, oat bran, pectin, and resistant starch as prebiotics. Infections, septic complications, mortality, days under ventilatory support, and days of stay in ICU were recorded. RESULTS: Synbiotic-treated patients exhibited a significantly reduced rate of infections (P = 0.01), SIRS, severe sepsis (P = 0.02), and mortality. Days of stay in the ICU (P = 0.01) and days under mechanical ventilation were also significantly reduced in relation to placebo (P = 0.001). CONCLUSION: The administration of this synbiotic formula in critically ill, mechanically ventilated, multiple trauma patients seems to exert beneficial effects in respect to infection and sepsis rates and to improve the patient's response, thus reducing the duration of ventilatory support and intensive care treatment.

Therapeutic fistuloscopy: an alternative approach in the management of postoperative fistulas.

BACKGROUND/AIM: Since the treatment of postoperative fistulas remains a difficult problem, we applied endoscopic treatment in such 14 persistent fistulas. METHODS: Fourteen patients presented with postoperative fistulas: 7 patients (low-output group) due to residual cavity after liver hydatid disease surgery and 7 patients (high-output group) after small-bowel resection (n = 3), diverted duodenostomy (n = 1), vertical gastroplasty (n = 1), external pancreatic cyst drainage (n = 1), and transduodenal sphincteroplasty (n = 1). The therapeutic procedures included mechanical removal of silk sutures, necrotic material, and hydatid membranes in the low-output group and fibrin sealing in the high-output group. RESULTS: Fistuloscopy was performed 170-278 days (mean +/- SD 198.7 +/- 36.7 days) and 18-51 days (mean +/- SD 34.0 +/- 11.3 days) postoperatively in low- and high-output fistula patients, respectively, when the average daily output was 20-50 (32.8 +/- 12.5) ml and 200-1,000 (563.1 +/- 319.4) ml, respectively. The low-output group needed only one fistuloscopy session, while the other group required a median number of three sessions plus fibrin sealing, the total amount of fibrin glue used per patient being 2-14 (6.5 +/- 4.4) ml. No procedure-related complication occurred. All fistulas except one healed within 10-33 (21.8 +/- 7.9) days and 2-17 (9.2 +/- 5.1) days in low- and high-output groups, respectively. CONCLUSIONS: We believe fistuloscopy to be a useful tool in the management of gastrointestinal fistulas, but more experience should be gained in using this technique.

The influence of continuous seven-day elevated intra-abdominal pressure in the renal perfusion in cirrhotic rats.

Since hepatorenal syndrome is a functional renal failure due to renal ischemia in cirrhotics with refractory ascites, we investigated whether increased intra-abdominal pressure (IAP) impairs the renal function and perfusion in cirrhotic portal hypertensive rats. Eight groups of 32 rats each were studied, including 4 control and 4 CCl(4) cirrhotic groups. These were subdivided into two groups each, with and without an increased IAP, and further subdivided into groups of rats with and without NO inhibition. IAP was increased to 20 mm Hg for 7 consecutive days by means of an intraperitoneally placed balloon filled with water. The animals were studied in normal conditions and after inhibition of NO synthesis. Changes in mean arterial pressure and renal microcirculation by means of femoral artery catheterization and laser-Doppler technique, respectively, were recorded. Venous samples for determination of plasma renin-aldosterone activity, biochemical parameters of liver and renal function, and plasma nitrite/nitrate levels as an index of NO synthesis were drawn. Cirrhotic rats showed decreased renal microcirculation (P = 0.05), while elevated IAP produced a further decrease (P = 0.01). Renin-aldosterone levels found increased (P = 0.001) in cirrhotics, and elevated IAP produced a further increase (P = 0.01] in both groups. Inhibition of NO synthesis resulted in a nonsignificant decrease in both renal microcirculation and renin-aldosterone levels in all experimental groups. Liver and renal function was found to be impaired in cirrhotics, but increased IAP had a nonsignificant further functional impairment in both organs. In conclusion, chronically elevated IAP in cirrhotic rats is associated with an increase in renin-aldosterone levels and significant impairment of renal perfusion.