Comparing Lavage of the Peritoneal Cavity with Lidocaine, Bupivacaine and Normal Saline to Reduce the Formation of Abdominal Adhesion Bands in Rats.

BACKGROUND: Intra-abdominal adhesions are fibrous bands that develop after abdominal surgery or inflammation and cause mortality and morbidity following surgeries. This study aimed to assess the effects of bupivacaine, saline and two doses of lidocaine, after peritoneal lavage and to compare their effects in reducing abdominal adhesions in rat. METHODS: In a blinded, randomised, placebo-controlled clinical trial, 50 female rats were anaesthetised and the parietal peritoneum was scratched to induce punctate bleeding. The rats were randomly assigned to five groups: saline, lidocaine 2% (3 and 6 mg/kg), bupivacaine 0.25% (2 mg/kg) and control (no irrigation). The peritoneal cavity was irrigated with the appropriate solution during laparotomy. Two weeks later, re-laparotomy was performed. The quantity, quality, severity and scores of adhesions were recorded and compared. RESULTS: The quantity and quality of adhesions were significantly higher in the control group than in the lidocaine (6 mg/kg) and bupivacaine groups. The quality of the adhesions was higher in the normal saline group than in the lidocaine (6 mg/kg) and bupivacaine groups. The severity of adhesions between the lidocaine 3 and 6 mg/kg groups and between the lidocaine 3 mg/kg and saline groups was lower than that in the control group. CONCLUSION: Using lidocaine (6 mg/kg) and bupivacaine lavage in first laparotomy reduces abdominal peritoneal obstruction because of the formation of adhesion bands.

Lovastatin prevents bleomycin-induced DNA damage to HepG2 cells.

Lovastatin as a member of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors is used as a lipid-lowering agent. It can also inhibit the formation of hydrogen peroxide and superoxide anion and finally leads to decline in oxidative stress processes. Here, we evaluated whether lovastatin can increase DNA damage resistance of HepG2 cells against genotoxicity of the anticancer drug bleomycin (BLM). HepG2 cells were incubated with different concentrations of lovastatin (0.1, 0.5, 1, 5 µM) before exposure to BLM (0.5 µg/mL for one h). The genotoxic dose of BLM and lovastatin was separately determined and comet assay was used to evaluate the genotoxicity. After trapping cells in agarose coated lames, they were lysed and the electrophoresis was done in alkaline pH, then colored and monitored by florescent microscope. The results of this study indicated that lovastatin in doses lower than 5 µM has genoprotective effect and in doses higher than 50 µM is genotoxic. In conclusion, lovastatin is able to protect genotoxic effects of BLM in HepG2 cells. Further studies are needed to elucidate the mechanism(s) involved in this process.