Signs of reperfusion injury following CO2 pneumoperitoneum: an in vivo microscopy study

During laparoscopic surgery, pneumoperitoneum is generally established by means of carbon dioxide (CO(2)) insufflation which may disturb hepatic microperfusion. It has been suggested that the desufflation at the end of the procedure creates a model of reperfusion in a previously ischemic liver, thus predisposing it to reperfusion injury.

To study the effects of pneumoperitoneum on hepatic microcirculation, Sprague-Dawley rats underwent pneumoperitoneum with an intraabdominal pressure of 8 or 12 mmHg for 90 min. Subsequently, in vivo microscopy was performed to assess intrahepatic microcirculation and transaminases were measured to index liver injury.

A CO(2) pneumoperitoneum of 8 mmHg did not change serum transaminases; however, further increase of intraperitoneal pressure to 12 mmHg significantly increased AST, ALT, and LDH measured after desufflation to almost 1.5 times as much as control values of 49 +/- 5 U/L, 31 +/- 3 U/L, and 114 +/- 12 U/L. In parallel, in all subacinar zones the permanent adherence of both leukocytes and platelets to the endothelium increased by about sixfold and threefold, respectively. Furthermore, Kupffer cells labeled with latex beads as an index for their activation were significantly increased compared to controls.

This in vivo observation demonstrated traces of reperfusion injury in liver induced by the insufflation and desufflation of CO(2 )pneumoperitoneum. The clinical relevance of this finding and the issue of using hepatoprotective substances to prevent this injury should be further investigated.