Intestinal prostaglandin E2 expression in rats with obstructive jaundice.

AIM: How obstructive jaundice causes the intestinal barrier to be injured is still controversially discussed. In this study, we hypothesize that intestinal prostaglandin E (2), a cytoprotective factor, may be affected by the bile duct obstruction. MATERIALS AND METHODS: Four groups of Wistar-Albino rats were used: in Groups 1 and 3, the rats underwent a sham operation. In Groups 2 and 4, the common bile duct was doubly ligated. Relaparotomy was performed after one week in Groups 1 and 2, and after two weeks in Groups 3 and 4, and specimens of the jejunum, ileum and liver were obtained for intestinal PGE (2) analysis and histopathological evaluation. RESULTS: Jejunal and ileal PGE (2) levels had significantly decreased in two-week bile duct-ligated rats compared to one-week ligated rats and the sham group (p < 0.01). Tissue injury scores (Chiu score) of the ileum were significantly higher in the two-week and one-week ligated rats than in the controls (p < 0.01 and p < 0.05, respectively). The jejunal injury score was significantly higher in the two-week ligated rats compared to controls (p < 0.05). The ileal and jejunal injury scores were higher in the two-week ligated rats than in the one-week ligated rats (p < 0.01 and p < 0.05, respectively). Precirrhotic fibrosis was detected in all two-week ligated rats, but in only 7 of 10 one-week ligated rats. CONCLUSIONS: Obstructive jaundice associated with intestinal tissue injury and precirrhotic changes leads to reduced intestinal PGE (2)-levels, suggesting an adverse effect on the intestinal cytoprotective process.

Lung re-expansion and urinary lipid peroxidation in neonatal pneumothorax.

AIM: Experiential studies suggest that re-expansion of a collapsed lung may result in pulmonary ischaemia-reperfusion injury. We aimed to evaluate the effect of lung re-expansion on urinary lipid peroxidation products in neonates with pneumothorax. METHODS: This study included 20 mechanically ventilated neonates with pneumothorax, and 18 healthy neonates (controls). A chest tube was inserted immediately following the diagnosis of pneumothorax. Urine samples were obtained just before tube thoracostomy (first period), after one hour (second period), every 12 hours by complete reexpansion (third period). Vital signs and ventilatory parameters were recorded. Urinary lipid peroxidation was evaluated by measurement of thiobarbituric acid-reacting substances (TBARS). RESULTS: No significant difference was found between urinary TBARS concentrations in the first, second and third periods (4.08 +/- 2.4 nmol/L, 2.8 +/- 2.3 nmol/L and 3.3 +/- 2.1 nmol/L, respectively). Control TBARS levels (4.1 +/- 2.1 nmol/L) did not significantly differ from those of the neonates with pneumothorax (p > 0.05). The neonates with pneumothorax had higher heart rates compared to the controls (p < 0.01). When compared with controls, the systolic pressure was lower in all periods (p < 0.01), and diastolic blood pressure was lower only in the first and second period (p < 0.05). Oxygen saturation significantly decreased in the first period compared to saturation of the second period and of controls (p < 0.01). Ventilatory parameters did not show any significant difference between the periods. CONCLUSIONS: This prospective study showed that re-expansion of the lung did not significantly affect urinary TBARS concentration in neonatal pneumothorax. Indirectly, short-term lung collapse followed by re-expansion might not cause a clinically significant reperfusion injury in newborns.