Table 3.
Level | Flow | Regulation | Effect of intervention |
---|---|---|---|
Systemic50,98,99 | Total HBF | ↓ in HBF seen with: ▪ ↓ CO ▪ ↓ SVR (other than splanchnic) ▪ ↑ RAP > PVP |
Inflow occlusion results in: ▪ MAP and ↓ CVP ▪ ↓ Blood loss Hepatic venous exclusion: ▪ Well tolerated ▪ ↓ CVP and CO ▪ MAP maintained >55 mmHg as a result of ↑ in SVR Infrahepatic caval clamping: ▪ Well tolerated ▪ ↓ Blood loss |
Regional50,66,100,101 | Total HBF | Total HBF (constant) = HAF + PVF (hepatic arterial buffer response) | Inflow occlusion followed by reperfusion results in ▪ ↓ SVR: ▪ Total HBF constant When preconditioning used: ▪ Total HBF Laparoscopic surgery: ▪ No difference in effect of inflow occlusion using laparoscopic or open surgery |
PVF | Passively drains splanchnic arterial bed so ↓ splanchnic flow results in ↓ PVF | Inflow occlusion followed by reperfusion results in: ▪ 29% ↓ in PVF on reperfusion lasting >30 min When preconditioning used: ▪ No change in PVF |
|
HAF | No auto-regulatory activity ↓ HAF with ↑ arterial resistance Arterial resistance ↑ with ↑ PVF (hepatic arterial buffer response) |
Inflow occlusion followed by reperfusion results in: ▪ 8% ↑ in HAF on reperfusion lasting >30 min When preconditioning used: ▪ 200% ↑ in HAF |
|
Micro50,66 | HSF | Flow controlled by diameter of the sinusoids Sinusoidal diameter controlled by sinusoidal endothelial cells, hepatic stellate cells and Kupffer cells |
Ischaemia and subsequent reperfusion create a mismatch in time and space of mediator release so that homeostasis of the mediators is lost |
Mediators released by above cells alter degree of contraction or relaxation of the cells, thus altering sinusoidal diameter and hence resistance to flow |
CO, cardiac output; CVP, central venous pressure; HAF, hepatic artery flow; HSF, hepatic sinusoidal flow; MAP, mean arterial pressure; PVF, portal blood flow; PVP, portal blood pressure; RAP, right atrial pressure; SVR, systemic vascular resistance.