sb-366791 and Liver-Diseases

Laparoscopic surgery induces a milder inflammatory response than open surgery, however, the precise mechanisms underlying this phenomenon remain to be elucidated. Our previous study demonstrated that stimulation of sensory neurons inhibited hepatic apoptosis and inflammatory responses in rats subjected to hepatic ischemia/reperfusion (I/R). Since carbon dioxide (CO2) has been demonstrated to stimulate sensory neurons, it was hypothesized that CO2‑pneumoperitoneum, as used in laparoscopic surgery, may attenuate inflammatory responses by stimulating sensory neurons. This hypothesis was examined using rats subjected to hepatic I/R. The rats were subjected to partial hepatic ischemia for 60 min followed by reperfusion. Abdominal insufflation with CO2 or air was performed for 30 min prior to hepatic I/R. Hepatic I/R‑induced hepatocellular apoptosis and expression of the neutrophil chemoattractant endothelial monocyte‑activated polypeptide‑II, were inhibited by CO2‑pneumoperitoneum, however, not by air‑pneumoperitoneum. Pretreatment with the transient receptor potential vanilloid 1 antagonist SB366791 reversed the protective effects of CO2‑pneumoperitoneum. The results from the present study demonstrated that CO2‑pneumoperitoneum attenuates hepatic apoptosis and inflammatory responses in rats subjected to hepatic I/R, possibly by stimulating sensory neurons. These findings suggested that CO2‑pneumoperitoneum contributed to the attenuated inflammatory response observed following laparoscopic surgery.

Topics: Anilides; Animals; Apoptosis; Carbon Dioxide; Cinnamates; Inflammation; Laparoscopy; Liver; Liver Diseases; Male; Pneumoperitoneum, Artificial; Rats; Rats, Wistar; Reperfusion Injury; Sensory Receptor Cells; TRPV Cation Channels