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Abstract
Hepatic dysfunction after portacaval shunting (PCS) has been attributed to loss of
portal perfusion to the liver. Proponents of selective systemic shunting state that
reduced encephalopathy and hepatic dysfunction with this procedure result from the
maintenance of portal perfusion to the liver through the hypertensive mesenteric venous
circulation. We questioned the importance of maintaining the diminished portal flow
to the cirrhotic liver because hepatofugal flow is known to develop in many of these
patients. We sought to further define mechanisms that may contribute to the maintenance
of critical flow to the liver in compensated hepatic cirrhosis. We demonstrated a
primary relationship between mesenteric venous hypertension (MVH) and increased hepatic
arterial blood flow after diversion of portal blood flow. Fifteen dogs had vena caval
stenosis above an end-to-side PCS to establish MVH and deprive the liver of portal
blood flow. Another 15 dogs had end-to-side PCS alone. A half hour after shunting,
hepatic arterial blood flow had increased significantly in all dogs. Hemodynamic parameters
remained stable throughout. Six weeks later, mesenteric pressure increased 98% ± 3%
with intracaval stenosis (from 9.6 ± 0.1 to 19.0 ± 0.3 cm H2O). Mesenteric pressure was unchanged with PCS alone (9.0 ± 0.1 cm H2O). Increased hepatic arterial flow was significantly elevated in all dogs above pre-shunt
values by 6 weeks postshunt. With MVH, however, further augmentation in hepatic arterial
flow was noted in the chronic state (1.5 ± 0.1 vs 0.9 ±0.1 ml/min/gm, p < 0.05). There
was significant correlation between MVH and increased hepatic arterial flow in the
chronic state (r = 0.79, p = 0.05). Hepatic arterial flow 6 weeks after PCS with MVH
was associated with lower blood ammonia and improved hepatocellular function compared
with animals with PCS alone. These results support the hypothesis that MVH is important
in maintaining blood supply—beyond providing driving force for sustained portal flow
to the liver. This is an important consideration in the medical and surgical management
of portal hypertension, a condition in which profound reduction in portal pressure
may negatively affect compensatory hepatic arterial blood flow.
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Article info
Publication history
Accepted:
January 18,
1989
Footnotes
☆This investigation was supported in part by the Alvin Baldwin, Jr., Chair in Surgery.
Identification
Copyright
© 1989 Published by Elsevier Inc.