Hepatic surgery in man often requires a transient interruption of the
blood flow to the liver. After the vascular declamping the hepatic rep
erfusion induces a group of phenomena commonly called ''reperfusion in
juries.'' The aim of this study was to evaluate the presence and effec
t of vasoactive agents that could induce the acute pulmonary arterial
hypertension which contributes to reperfusion injury, Wister rats were
used. The hepatic ischemia was induced by cross-clamping the whole he
patic hilus for 20, 40, and 60 min, In control experiments a sham oper
ation was performed, Blood samples were collected from the suprahepati
c inferior vena cave, Strips of the main pulmonary artery were set up
in an isolated organ bath and tested for the response to noradrenaline
, adrenaline, KCl, and plasma samples. Plasma levels of catecholamines
were determined by high-performance liquid chromatography. Plasma con
centration of noradrenaline significantly increased from 1.6 +/- 0.4 (
control) to 10.8 +/- 2.9 ng . ml(-1) and adrenaline concentration rose
from 2.7 +/- 0.7 to 38.7 +/- 7.6 ng . ml(-1) after ischemia, Noradren
aline potency, compared to control values, significantly increased aft
er prolonged liver ischemia, The plasma samples collected after prolon
ged liver ischemia caused a greater contraction of the pulmonary arter
y than from control plasma. This contraction is partially inhibited by
phentolamine, We conclude that hepatic ischemia modifies the response
of the pulmonary artery to exogenous noradrenaline, At the same time
it induces an increase in the plasma levels of adrenaline and noradren
aline, The resulting combined effect may cause the pulmonary hypertens
ion which has been observed in reperfusion injury. (C) 1996 Academic P
ress, Inc.