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

Abstract

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 (PO2) 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 PO2 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 PO2 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. We investigated the effect of CO2-pneumoperitoneum on liver blood flow, hepatic tissue oxygenation (PO2) and liver enzyme release. CO2-insufflation reduces portal venous flow without a compensatory increase of hepatic arterial flow ("hepatic arterial buffer response"), resulting in reduced hepatic PO2 and increased ratios of serum alanine aminotransferase to serum aspartate aminotransferase.