Loss of physiologic hepatic blood flow control ("hepatic arterial buffer response") during CO2-pneumoperitoneum in the rat

We analyzed whether a compensatory increase of hepatic arterial (HA) flow, known as the "hepatic arterial buffer response" (HABR), may serve for maintenance of liver blood supply during laparoscopy-associated portal venous (PV) flow reduction. We assessed HA and PV flow, as well as hepatic tissue oxygenation (Po,) during CO2-pneumoperitoneum in anesthetized and mechanically ventilated Sprague-Dawley rats (n = 7). Control animals (n = 7) without pneumoperitoneum, but tourniquet-induced PV flow reduction served to demonstrate physiologic HABR. Although stepwise tourniquet-induced reduction of PV flow to 20% of baseline values led to a significant (P < 0.05) increase of HA flow from 4.3 +/- 0.7 mL/min to 9.9 +/- 1.7 mL/min, stepwise intraabdominal pressure-induced decrease of PV flow was paralleled by a linear reduction of HA flow from 2.4 :+/- 0.3 mL/min to 1.2 +/- 0.5 mL/min at 18 mm Hg intraabdominal pressure. This loss of HABR was sustained during a subsequent 2 h-period of CO2-pneumoperitoneum contrasting the 2 h of maintenance of HABR in controls. Hepatic tissue Po, decreased during the 2 h-period of pressure- and tourniquet-induced PV flow reduction by 35% to 51%, respectively. On tourniquet release, all variables regained baseline values, whereas evacuation of the pneumoperitoneum allowed all variables except hepatic Po-2 to return to baseline, indicating prolonged tissue hypoxia despite restored total liver blood flow in the Laparoscopic group. Concomitantly, increased liver enzyme activities reflected moderate tissue damage after 2 h of pneumoperitoneum. In conclusion, intraabdominal CO2-insufflation-induced hemodynamic alterations may impair tissue oxygenation and enzyme release, indicating the potential risk for hepatic tissue damage after prolonged periods of laparoscopic interventions.