Unilateral hepatic duct obstruction in the primate.
The effects of obstruction of one hepatic duct were investigated in two studies in the rhesus monkey. A model to divide bile flow from the two sides of the liver was developed in the first study. Bile flow from one side of the liver was obstructed and backflow from the obstructed biliary tract was investigated in five animals. Test solutions containing sulfobromophthalein (BSP) and conjugated cholic acid-14C were introduced into the obstructed side of the liver at pressures below and above the maximum secretory pressure. These solutes were detected in the circulation and in the bile on the free side of the liver. BSP, secreted on the free side, was conjugated normally (52.7 percent) for this species. There was also backflow of water from the obstructed side and continuing secretion into the obstructed side. It was determined that there were no functionally significant biliary communications between the two separately cannulated portions of the liver. In the second study, graded unilateral obstruction and recovery were studied in five animals. Bile flow, eyythritol-14C clearance, and bile acid, bilirubin, and bicarbonate secretion rates were reduced during obstruction and recovery. The bile:plasma ratio of erythritol-14C fell significantly (1.13 to 0.97) and the bicarbonate concentration increased during partial obstruction. On the free side, bile flow, erythritol-14C clearance, and bile acid secretion rates increased during obstruction. The increase in bile flow was due largely to an increase in canalicular bile acid-dependent flow. The studies indicated that reduced bile flow during acute obstruction is due to both hydrostatic backflow and secretory failure. The latter occurs mainly at the canalicular level, whereas the bile ductules are spared at least relatively. During acute obstructions compensations in unobstructed portions of the liver are due to increased secretion of solute at the canaliculus.
Strasberg
S M
SM
Department of Surgery, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada.
Petrunka
C N
CN
Ilson
R G
RG
D000818:Animals; D001646:Bile / Q000378:metabolism; D002779:Cholestasis / Q000209:etiology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004896:Erythritol / Q000378:metabolism; D005260:Female; D006500:Hepatic Duct, Common; D008253:Macaca mulatta; D011312:Pressure; D013448:Sulfobromophthalein
D013448:Sulfobromophthalein; D004896:Erythritol