Bile secretion (2): Bile secretion and obstructive jaundice

1968 ◽  
Vol 3 (1) ◽  
pp. 420-420
Author(s):  
S. Miwa ◽  
T. Ueno ◽  
M. Ohto ◽  
N. Kogure ◽  
T. Kuroda ◽  
...  
Keyword(s):  
Obstructive Jaundice ◽  
Bile Secretion

scholarly journals THE PATHOGENESIS OF ICTERUS

1911 ◽  
Vol 13 (1) ◽  
pp. 115-135 ◽  
Author(s):  
G. H. Whipple ◽  
J. H. King
Keyword(s):  
Obstructive Jaundice ◽  
Thoracic Duct ◽  
Bile Secretion ◽  
Pericardial Fluid ◽  
The Body ◽  
Chronic Obstructive ◽  
Bile Pigment ◽  
Bile Pigments ◽  
Secondary Factor ◽  
The Common

These experiments indicate that, in obstructive jaundice, the bile which escapes from the liver is absorbed by the hepatic capillaries and carried by the blood to the kidneys. The presence of a thoracic duct fistula influences in no way the development of icterus after total obstruction of the common bile duct. Bile pigments, sufficient to give a Salkowski test, may or may not appear in the lymph of the thoracic duct in such experiments, their appearance possibly depending upon the rapidity of bile secretion and the amount of lymph flow. Chronic icterus developing in an animal with a thoracic duct fistula gives an interesting distribution of bile pigments in the body fluids. The lymph and pericardial fluid contain the same amount, which is much less than the content of bile pigment in the blood serum and urine. It seems clear that in both acute and chronic obstructive jaundice the lymphatic apparatus takes no essential or active part in the absorption of bile pigments from the liver. At best, the lymphatic system is a secondary factor in the mechanism of jaundice.

Studies on bile secretion (III) the uptake, conjugation and excretion of bile pigments by the liver under the obstructive jaundice

1968 ◽  
Vol 3 (4) ◽  
pp. 298-298
Author(s):  
S. Miwa ◽  
T. Ueno ◽  
M. Ohto ◽  
G. Takazawa ◽  
Y. Kuniyasu ◽  
...  
Keyword(s):  
Obstructive Jaundice ◽  
Bile Secretion ◽  
Bile Pigments

Additional evidence for AQP1 vesicle trafficking as a molecular mechanism for ductal bile secretion

2001 ◽  
Vol 120 (5) ◽  
pp. A91-A91
Author(s):  
P TIETZ ◽  
P SPLINTER ◽  
M MCNIVEN ◽  
R HUEBERT ◽  
N LARUSSO
Keyword(s):  
Molecular Mechanism ◽  
Vesicle Trafficking ◽  
Bile Secretion

Indications for Surgical Exploration in the Diagnosis of Intrahepatic Obstructive Jaundice

1952 ◽  
Vol 22 (2) ◽  
pp. 232-243
Author(s):  
Leonard A. Stine ◽  
Richard M. Bendix ◽  
Jerome M. Swarts
Keyword(s):  
Obstructive Jaundice ◽  
Surgical Exploration

Impaired Fibrinolysis in Obstructive Jaundice - Evidence from Clinical and Experimental Studies

1988 ◽  
Vol 60 (01) ◽  
pp. 025-029 ◽  
Author(s):  
M Colucci ◽  
D F Altomare ◽  
G Chetta ◽  
R Triggiani ◽  
L G Cavallo ◽  
...  
Keyword(s):  
Renal Failure ◽  
Bile Duct ◽  
Obstructive Jaundice ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Experimental Studies ◽  
Plasminogen Activator Inhibitor ◽  
Venous Stasis ◽  
Microvascular Thrombosis ◽  
Duct Ligation

SummaryMicrovascular thrombosis is considered an important pathogenetic factor in renal failure associated with obstructive jaundice but the mechanisms leading to fibrin deposition are still unknown. The plasma levels of plasminogen activator inhibitor (PAI) in 29 patients with obstructive jaundice were found significantly increased as compared to 20 nonjaundiced patients. Fibrin autography of plasma supplemented with tissue plasminogen activator (t-PA) revealed that in icteric samples most of the added activator migrated with an apparent Mr of 100 kDa, corresponding to t-PA-PAI complex, whereas in control samples virtually all t-PA migrated as free enzyme. PAI activity detected in icteric samples is similar to the endothelial type PAI since it is neutralized by a monoclonal antibody against PAI-1.Venous stasis in jaundiced patients was neither associated with an increase in blood fibrinolytic activity nor with a decrease in PAI activity. Immunologic assay showed that t-PA release was impaired in 3 out of 4 patients. In controls, venous occlusion induced an increase in both fibrinolytic activity and t-PA antigen and a reduction in PAI activity. Bile duct recanalization in jaundiced patients subjected to surgery was accompanied by a decrease in plasma PAI activity which paralleled the decrease in serum bilirubin levels. In nonjaundiced patients, surgical treatment did not cause significant changes in either parameter. Rabbits made icteric by bile duct ligation showed an early and progressive increase in plasma PAI activity indicating that obstructive jaundice itself causes the elevation of circulating PAI. It is concluded that obstructive jaundice is associated with a severe impairment of fibrinolysis which might contribute to microvascular thrombosis and renal failure.

Tuberculous Abscess of the Pancreas Presenting as Obstructive Jaundice: A Case Report

2002 ◽  
Vol 46 (6) ◽  
pp. 593 ◽  
Author(s):  
Dong Kyun Yoo ◽  
June Sik Cho ◽  
Kyung Sook Shin ◽  
Dae Young Kang
Keyword(s):  
Case Report ◽  
Obstructive Jaundice ◽  
Tuberculous Abscess
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