Am. J. Respir. Crit. Care Med., Vol 152, No. 2, 08 1995, 511-518.
Regional control of venous return: liver blood flow
N Brienza, T Ayuse, CP O'Donnell, S Permutt and JL Robotham
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21287-4965, USA.
The aim of the study was to determine whether closing pressures or vascular
distensibility can be used to describe liver venous hemodynamics when right
atrial pressure is raised. The study was performed using a vascularly
isolated pig liver preparation that allowed the independent control of
portal vein and hepatic artery inflows and of outflow pressure (Pout).
Pressure-flow (P-Q) relationships of both liver vessels were generated at
multiple levels of Pout. At Pout of 0 mm Hg, the portal vein P-Q
relationship was linear, with a convexity toward the pressure axis at low
flows (5 to 10 ml/min/kg). The zero flow pressure was 1.5 +/- 0.2 mm Hg,
greater than Pout (p < 0.05). On raising Pout from 0 to 15 mm Hg, the
shape of the portal vein P-Q relationships became progressively more
linear, with a decrease in slope; no difference between zero flow pressure
and Pout was observed. At Pout of 0 mm Hg, the hepatic artery presented a
zero flow pressure > Pout. Raising Pout from 0 to 15 and 30 mm Hg
resulted in a zero flow pressure always > Pout (p < 0.05). The
behavior of the liver vein system is characterized by a zero flow pressure
mimicking a classic vascular waterfall and by distensibility, once the
waterfall is exceeded. Both factors act to minimize the reduction in venous
return with an increased central venous pressure. Flow through the hepatic
artery is affected by an increase in backpressure occurring upstream from
the sinusoids, reducing arterial inflow for a constant perfusion pressure.
