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Results for “Jaundice, Obstructive”

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The perioperative changes in glomerular filtration and renal blood flow in patients with obstructive jaundice.

Experimental alterations in renal haemodynamics have been observed in obstructive jaundice and these may be the pathophysiological mechanism of increased renal susceptibility to injury in obstructive jaundice. Dynamic 99mTc-DTPA renal scintigraphy was done before and eight weeks after elective hepatobiliary surgery in six patients with obstructive jaundice (bilirubin greater than 100 mumol/l) and in six non-jaundiced control patients to assess changes in glomerular filtration and renal blood flow. Glomerular filtration was lower preoperatively in the jaundiced patients than in the control patients. Glomerular filtration increased postoperatively in jaundiced patients, but decreased in control patients. Renal blood flow was reduced postoperatively in control patients, but not in jaundiced patients. The changes in renal blood flow were different for each group of patients. These results provide clinical evidence of altered renal haemodynamics and a reversible impairment of glomerular filtration in obstructive jaundice. The changes seen in renal blood flow may be the underlying mechanism of increased renal susceptibility to injury.

Adult↗

[Experimental study on the pathogenesis of acute ulceration in obstructive jaundice--with reference to gastric mucosal blood flow].

We prepared obstructive jaundice models in rats in order to study the mechanism of acute ulceration in obstructive jaundice centering on impediments to gastric wall blood flow and changes in gastric mucosal NA and PGE2 when the rats were subjected to water immersion restraint stress. The results were: In the obstructive jaundice 2 weeks group, when subjected to water immersion restraint stress, gastric mucosal NA reached a dried up stage from the incipient stage, causing gastric mucosal impediments at the same time, showing a significant decrease of gastric mucosal PGE2. Intragastric pH was at a similar level of excessive acidity in all groups; gastric acid is believed to be a secondary factor promoting ulceration. Gastric mucosal PGE2 showed a significant decrease coinciding with the increase in ulceration index, being a possible factor of ulceration; it is also presumed to regulate gastric wall blood flow alternatively with gastric mucosal NA. Pre-treatment with PGE2 prior to loading stress resulted in a decrease in gastric wall blood flow being significantly controlled. The administration of PGE2 brought about an improvement in gastric wall blood flow and a consequent increase in gastric mucosal NA, being judged effective for acute ulceration in obstructive jaundice.

Acute Disease↗

[Hepatic protein synthesis and cytokines in obstructive jaundice].

UNLABELLED: To clarify the mechanism of the increase of hepatic protein synthesis observed in the obstructive jaundiced rats, hepatocellular protein synthesis (HPS) and secretory protein synthesis (SPS) were estimated in the rats with obstructive jaundice and the contents of the following in the peripheral blood were determined in 21 patients with obstructive jaundice before and two weeks after percutaneous transhepatic biliary drainage (PTBD): interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF alpha), endotoxin (Et), acute-phase protein (APP) and negative acute-phase protein (NAPP). THE RESULTS: (1) HPS and SPS were markedly increased by obstructive jaundice; (2) IL-1 beta and IL-6 were significantly high and were reduced after PTBD; (3) neither TNF alpha nor Et was detected; (4) APP were significantly high and failed to decline after PTBD; (5) NAPP were significantly low and the contents were restored to the normal levels after PTBD. These results suggest that increased hepatic protein synthesis observed in the rats with obstructive jaundice correspond to the increased hepatic production of APP in patients with obstructive jaundice.

Acute-Phase Proteins↗