Biomedical Engineering Reference
In-Depth Information
20.1 Introduction
The human liver receives its blood supply via the portal vein and the hepatic artery
and is drained via the hepatic vein. The supplying and draining systems are con-
nected via a delicate, highly organized vascular network. This vascular network con-
sists of specific capillaries called sinusoids. Sinusoids are evenly distributed among
liver cell plates, giving the liver 'sponge-like' properties.
Further, blood supply to the liver is delivered via two main branches of the portal
vein and hepatic artery. These branches are the right and left portal vein, respec-
tively, the right and left hepatic artery. Venous drainage of the liver is ensured by
three hepatic veins, called the right, middle, and left hepatic veins. This two-to-three
imparity is the anatomical basis of the focal outflow obstruction induced by resect-
ing half of the liver. This surgical procedure is performed in extended liver resection
and split liver transplantation. Resecting half of the liver requires the transection of
the middle hepatic vein, leading to an outflow obstruction in the dependent hepatic
territories.
Focal outflow obstruction induces hepatocellular damage in the respective drai-
nage territories, leading to additional loss of functional liver tissue. This loss of
functional liver mass adds to the loss caused by the resection itself. This combined
loss of functional live mass can be detrimental for the patient undergoing extended
liver resection, causing a small probability for size syndrome or even death. Liver
resection itself causes portal hypertension, as half of the vascular bed is removed,
forcing all blood from the intestine through a reduced vascular bed.
In Ricken et al. (
2010
) it was demonstrated that the proposed model applies to
impaired perfusion of the liver after inducing focal outflow obstruction and the sub-
sequent reestablishment of hepatic venous drainage. For the two-dimensional case,
the results are closely compared to the results obtained in parallel, specifically de-
signed experiments using our newly developed surgical model.
We created a surgical model of focal outflow obstruction in a rat, see Fig.
20.1
.
The rat liver consists of a median lobe which is—as is the human liver—supplied
by two vessels, but drained by three vessels, and an additional three lobes supplied
and drained separately. We incorporated focal outflow obstruction by ligating the
right median hepatic vein and performed an additional 50 resection by removing
the left lateral lobe to induce portal hypertension, cf. Dirsch et al. (
2008
). We were
able to observe the extent of primary hepatic damage in the outflow obstructed area
as well as the spontaneous recovery process consisting of reestablishment of ve-
nous drainage and parenchymal recovery from outflow obstruction. Further, volume
recovery by growth of the liver (
=
regeneration) after liver resection was also ob-
served.
Hepatic-venous drainage was reestablished within hours after ligation by redi-
recting sinusoidal blood flow via multiple-dilated sinusoids into the unobstructed
neighboring territories. Within seven days the high number of dilated sinusoids was
reduced to single vascularized sinusoidal canals. We postulated that the pressure
gradient from the congested area to the neighboring normally drained territory in
the hepatic 'sinusoid sponge' was the driving force for the formation of vascular
