AJP - Heart and Circulatory Physiology, Vol 246, Issue 5 658-H663, Copyright © 1984 by American Physiological Society
Loss of hepatic venous responsiveness after endotoxin in anesthetized cats
K. L. Seaman and C. V. Greenway
Endotoxin (from Salmonella enteriditis ) was administered either as an
intravenous bolus injection after administration of indomethacin to prevent
the acute anaphylactoid response or as a slow intravenous infusion to cats
anesthetized with pentobarbital. Within 30 min, hepatic blood volume
measured by plethysmography increased by 30%. However, unlike the outflow
block seen in dogs after endotoxin, this increase in blood volume was
associated with a fall in portal and hepatic lobar venous pressures.
Responses to hepatic nerve stimulation (1-8 Hz), to intravenous infusions
of norepinephrine (0.2-1.0 microgram X kg-1 X min-1), and to infusions into
the hepatic artery of norepinephrine (0.1-0.5 microgram X kg-1 X min-1) and
angiotensin II (0.1-0.5 microgram X kg-1 X min-1) were compared before and
150 min after endotoxin administration. Both portal pressure and hepatic
blood volume responses to these stimuli were markedly depressed by 150 min
after endotoxin. We conclude that in cats endotoxin causes a markedly
depressed responsiveness of hepatic venous smooth muscle to agonists and a
modest pooling of blood in the liver probably due to impairment of
preexisting sympathetic tone. Although these hepatic venous effects were
observed at a time when cardiac output was not markedly depressed, it is
suggested that they may play a significant role in the later development of
reduced cardiac output and shock.
