Biomedical Engineering Reference
In-Depth Information
4 Hemodynamics and the Liver
4.1 Blood Flow in the Liver
The liver is the body's most important metabolic organ and plays a central role in
detoxifying blood-transported components. The liver has a unique dual circula-
tion system, receiving 75 % of its oxygenated blood from the hepatic portal vein
and 25 % from the hepatic artery. Each of these two vessels provides about half
of the liver's oxygen requirement. The hepatic artery provides arterial blood,
whereas the hepatic portal vein is responsible for transporting the venous blood
from the spleen and the gastrointestinal tract, and its associated organs. In
humans, both hepatic lobes are composed of about a million small lobules that
are a maximum of 1-2 mm in size. Blood entering the liver flows through
morphologically sinusoidal microvessels surrounded by hepatocytes and drains
into a centrally located vein. This exceptional architecture ensures that the blood
is brought into best possible contact with the hepatocytes when it flows through
the organ. These veins then merge into the hepatic vein, which drains the blood
out of the liver.
Blood flow subjects the endothelial cells to two major complex hemodynamic
forces. The cyclic strain that results from mechanical distortion and tension of a
vessel's wall, caused by the pumping action of the heart, affects the vascular
cells. The shear stress, due to the frictional force that results from viscous blood
flow over the vessel lumen, is imparted onto the endothelial cells lining the
vessel's lumen. Blood pressure is the major determinant of cyclic stretch, while
shear stress is determined by the blood flow, viscosity, and the diameter of the
blood vessel. The liver's capacity to withstand vascular stress is illustrated
through its management of blood flow following PH. Following a 2/3 PH, all
blood provided by the hepatic portal vein is shunted to the remaining one-third of
the liver, effectively tripling the incoming blood flow rate and volume, causing
acute portal hypertension. This increase in blood flow is achieved by circum-
ferential vessel wall expansion resulting in the stretching of endothelial cells and
other cell types in the vessel wall. The liver lacks the ability to control the
volume of portal blood flow despite it comprising up to 75 % of total liver intake.
It is reasonable to postulate that the increase in blood volume entering the liver
following partial hepatectomy may play a role in triggering the rapid regeneration
of the liver. The cellular response to this stress may be mediated through
mechanotransduction. Interestingly, when portal blood flow is experimentally
deprived, a compensatory increase of arterial blood supply, known as the hepatic
arterial buffer response (HABR), occurs. This phenomenon implicates that the
abrupt shift in blood flow distribution after partial hepatectomy is a first-line
trigger
to
provoke
the
regeneration
process,
while
regeneration
is
halted
following the gradually normalized blood flow.
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