Abstract

INTRODUCTION: The CAVESWave® organ perfusion system provides cardio-emulated systolic and diastolic pressure waves to the hepatic artery HA, as well as variable pressure to the portal vein PV, replicating in vivo hepatic perfusion conditions. This allows a unique opportunity to study the interaction between HA and PV flow patterns in the autoregulation of hepatic venous HV outflow. The conditions exclude artefacts generated from cardiac pulsations. METHODS: Ten freshly procured porcine livers were perfused on the CAVESWave® system for four hours. At the two-hour midpoint, the temperature of the perfusate was increased from 15°C to 30°C and the flow variation associated with the temperature change documented. Flow rates in the HA, PV and HV were captured using flow sensors in the perfusion circuit. The distribution of perfusate was documented using Infra-red thermography (IRT), which measured surface liver temperature to a depth of 3 mm. RESULTS: Both IRT and the flow sensor measurements demonstrated stable, steady-state values after target perfusate temperatures were reached. Pulsatile waves reflecting cardio-emulated systolic and diastolic pressure waves were present in both HA (Figure 1) and PV (Figure 2). The only possible source of pulsations in the PV was transmission from the HA. Pulsatile waves were significantly attenuated or absent in the HV (Figure 3). The flow at 150 C in the HA (630.1 + 239.9; ml/min M + SD) was significantly greater than in the PV (316.2 + 90; P < 0.004). As expected, flow in the HV (904 + 292.8) approximated the sum of HA and PV flow. Increasing the temperature of the perfusate to 300 C significantly increased flow in all three circuits: HA (761.5 + 220; P < 0.014); PV flow (375.0 + 139.1; P < 0.007) and HV (1016.1 + 302.4; P < 0.007). The flow in the HA increased by 116.75 + 140.9 ml/min; the increase was 56.7 + 80.3 in the PV and 111.8 + 100.8 in the HV. The time for this change was significantly shorter for HA (18.9 + 13.5 mins) than for PV (26.4 + 18.1; P < 0.05). The significance of the delay in the PV flow is unclear. It likely reflects greater capacitance within the venous circuit. PV flow was inversely correlated with HA flow at all temperatures, correlation coefficient, -0.26. This suggests compensation or buffering between the arterial and venous circuits. CONCLUSION: Autoregulation of flow in response to temperature change is maintained in the ex vivo perfused liver. The inverse correlation between HA and PV flow, suggests a Hepatic Artery Buffering Response, HABR in this model.

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