Perfusion of the Dog Pancreas with Bile Without Production of Pancreatitis

White, Thomas Taylor; Magee, D. F.

doi:10.1097/00000658-196002000-00014

Cited by 43 publications

(20 citation statements)

References 3 publications

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“…Contamination of bile by enteric organisms seen after biliodigestive anastomosis has no pathological consequences on the intrahepatic bile duct system as long as the outflow occurs unimpeded. Further more, experimental rerouting of bile with and without infection through the pancreas does not result in pancre-atitis if intraluminal pressures remain in a physiological range [11][12][13].…”

Section: Ductular Pathways Of Infectionmentioning

confidence: 99%

Is Bile a Source of Infection in Acute Pancreatitis?

Senninger¹

1996

Dig Surg

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Infection of bile is one of the consequences of acute cholecystitis and bile duct obstruction. Its contribution to infection of pancreatic necrosis, despite its theoretical relevance, remains unclear. However, biliary obstruction leads to both increased bacterial translocation and reticuloendothelial system dysfunction resulting in a net increase in circulating bacteria and endotoxin. It is via this indirect mechanism that bile, infected or not, may contribute most to the infectious processes in acute pancreatitis.

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Section: Ductular Pathways Of Infectionmentioning

confidence: 99%

Is Bile a Source of Infection in Acute Pancreatitis?

Senninger¹

1996

Dig Surg

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“…The mechanism by which stone passage triggers acute pancreatitis is still a subject of discussion. The Opie theory has been challenged by reports that bile can be infused through the pancreas at physiologic pressures without causing pancreatitis 19,20 and that a common channel is present in only a small percentage of the population. 21 Further, it has been observed that pancreatic ductal pressure exceeds biliary ductal pressure, 22 suggesting that even if a common channel existed, reflux of pancreatic juice into the bile duct rather than flow of bile into the pancreas would be expected.…”

Section: Discussionmentioning

confidence: 99%

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

Schleicher¹,

Baas²,

Elser³

et al. 2001

Annals of Surgery

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ObjectiveTo examine the relation between hepatic reticuloendothelial system (RES) dysfunction and the development of acute biliary pancreatitis. In an opossum model, the authors tested the hypothesis that RES blockade can turn the mild pancreatitis seen after pancreatic duct obstruction (PDO) into the severe form. Summary Background DataBiliary obstruction is considered the decisive event in gallstone pancreatitis. Suppression of the RES occurs during biliary obstruction. MethodsEighteen opossums were placed into three groups of six animals each: group A, RES blockade with -carrageenan; group B, PDO; and group C, PDO and RES blockade with carrageenan. The severity of pancreatitis was evaluated by enzyme serum levels and percentage of pancreatic tissue necrosis. RES capacity was measured by dynamic liver scintigraphy, and hepatic blood flow was documented using the hydrogen clearance technique. ResultsNo changes in hepatic blood flow occurred in groups A to C. RES capacity was suppressed in groups A and C; in group B, RES function remained unchanged. In group A, amylase and lipase levels remained normal, 3 Ϯ 1.9% of pancreatic tissue were necrotic. The animals in group B developed mild edematous pancreatitis with an increase in amylase and lipase levels and 15 Ϯ 10% of pancreatic necrosis. In group C, amylase and lipase increased significantly and histology revealed severe necrotizing pancreatitis, with 72 Ϯ 11% of necrotic areas. ConclusionsArtificial RES blockade can promote the progression from mild pancreatitis as observed after PDO to the severe necrotizing form of the disease. Thus, RES dysfunction resulting from biliary obstruction might be an important cofactor in the pathogenesis of bile-induced pancreatitis.Acute biliary pancreatitis is an inflammatory disease that varies in severity and outcome. Mild edematous pancreatitis usually results in morphologic and functional recovery, whereas severe necrotizing pancreatitis is often associated with multisystemic complications and a death rate of 10% to 50%. 1 The reason for this variety in manifestation is not known. The identification of factors determining the severity of acute pancreatitis is essential to improve the understanding of the pathophysiology of bile-induced pancreatitis and its complications.Obstruction of the terminal biliopancreatic ductal system is considered to be the triggering event in human gallstone pancreatitis. Opie, 2 in 1901, postulated that reflux of bile, caused by a gallstone impacted in a common terminal biliopancreatic duct, initiates the process of pancreatic inflammation. Today, most authors disagree with this socalled common channel theory, and not reflux of bile but simultaneous obstruction of the biliary and the pancreatic ducts and their pathophysiologic consequences are considered to be the determining factors in the development of severe pancreatitis.

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“…Since these solutions contain trypsin and chymotrypsin, they cause destruction of the pancreatic tissues by enzymatic digestion, thus initiating the inflammatory response. Experimental pancreatitis has been induced by injection of saline and a variety of irritating materials into the pancre as at greater than normal pressure [15,24,37]. Reflux without increase in pressure is not pathogenic, as bile passing through the small intestine into the gland under normal pressure does not cause pancreatitis [28].…”

Section: Discussionmentioning

confidence: 99%

Factors in the Pathogenesis of Experimental Acute Pancreatitis in the Rat

Durst¹,

Dishon²,

Rosenmann³

et al. 1973

Eur Surg Res

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This is a study of the injurious effects of transient reflux of diverse solutions when introduced into the pancreas of rats under pressure through the obstructed duodenum. Mild pan Immune complex disease creatitis resulted from introduction of saline. Administration of homologous or heterologous proteinaceous solutions induced moderate pancreatitis; prior sensitization of the animals to the respective protein did not aggravate the inflammatory process. Severe pancreatitis developed after intraduodenal injection of nephrotoxic serum (basement membrane antibodies) or preformed immune complexes. It is suggested that pancreatitis ensues as a result of reflux of solutions carrying activators of trypsinogen from the duodenum into the ducts at a time when pancreatic secretion is enhanced by intestinal hormones. Pancreatic damage results from passage of the activated enzymes across the acinar and ductular epithelium into the interstitial tissue. The severity of the pancreatitis is augmented when immune mechanisms are superimposed. An attempt at demonstrating organ-specific antigens in the urine of rats with pancreatitis was unsuccessful.

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Perfusion of the Dog Pancreas with Bile Without Production of Pancreatitis

Cited by 43 publications

References 3 publications

Is Bile a Source of Infection in Acute Pancreatitis?

Is Bile a Source of Infection in Acute Pancreatitis?

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

Factors in the Pathogenesis of Experimental Acute Pancreatitis in the Rat

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