PubMed2003
BACKGROUND: Pneumoperitoneum (P) created to facilitate laparoscopy (L) is associated with splanchnic perfusion, ischemia/reperfusion (I/R) injury, and oxidative stress. In this randomized controlled experimental study with blind outcome assessment, we evaluated the effect of preconditioning (PRE) on L-induced I/R injury. METHODS: The subjects were 40 Sprague-Dawley male rats. P was created in all except controls, using carbondioxide (CO2) insufflation under a pressure of 15 mmHg. PRE consisted of 10 min of P, followed by 10 min of deflation (D). The rats were randomized to the following groups: Group P was subjected to 60 min of P. Group P/D was subjected to 60 min of P, followed by 45 min of D. Group PRE/P was subjected to PRE, followed by 60 min of P. Group PRE/P/D was subjected to PRE, followed by 60 min of P and 45 min of D. Group C (control) was subjected to a sham operation, without P. Its anesthesia time was equal to that for group PRE/P/D. At the end of the experiments, the rats were killed; blood, liver, and kidney samples were then obtained and coded. Plasma alanine aminotransferase (ALT) and malondialdehyde (MDA), as well as homogenized tissue MDA levels and glutathione (GSH) activities, were measured; tissue samples were assessed for histopathological evidence of injury; all assessments were done by investigators blinded to the study design. The results were decoded and analyzed statistically with the Kruskal-Wallis and Mann Whitney tests. A p <0.05 was considered significant. RESULTS: Plasma ALT as well as plasma, liver, and kidney MDA levels and liver and kidney injury scores were increased, whereas liver and kidney GSH values were decreased in groups P and P/D, as compared to group C. Rats subjected to PRE before P had plasma ALT, kidney MDA, and kidney and liver GSH levels comparable to controls; their kidney and liver injury scores were higher than controls but significantly lower than nonpreconditioned animals. PRE enabled decreased plasma, kidney, and liver MDA as well as increased kidney GSH if applied before P; its efficacy on oxidative stress was limited to providing decreased kidney MDA and increased kidney GSH if applied before P/D. However, PRE significantly attenuated kidney and liver injury after P as well as P/D. CONCLUSION: PRE consisting of 10 min of P followed by 10 min of D decreases the oxidative stress induced by sustained P in the plasma, liver, and kidney. PRE significantly limits liver and kidney injury after prolonged P and P/D. After further studies to define its ideal timing, PRE before L incorporating P may have clinical relevance, especially for elderly patients or those with impaired hepatic and/or renal function or perfusion.