Importance of Microcirculatory Disturbances in the Pathogenesis of Pancreatitis

Uhlmann, Dirk; Ludwig, Stefan; Geißler, Felix; Tannapfel, Andrea; Hauss, Johann; Witzigmann, Helmut

doi:10.1055/s-2001-19157

Cited by 26 publications

(13 citation statements)

References 58 publications

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“…Both the accumulation of activated coagulation factors and decreased reticuloendothelial clearance maintained the formation of microthrombi and associated microvascular disturbances, resulting in the functional impairment of several organs (25). Pancreatic microvascular control is a complex and incompletely understood physiological process (26). Blood flow in the pancreas is altered by a large number of endogenous and exogenous factors.…”

Section: Discussionmentioning

confidence: 99%

“…Blood flow in the pancreas is altered by a large number of endogenous and exogenous factors. In acute pancreatitis reduction in blood flow and alterations of microvascular integrity resulting in impaired tissue oxygenation play an important role in the initiation and progression of the disease (7,(26)(27)(28). Inhibition of endothelium-derived relaxing factor by free heme may cause a local vasoconstriction of the pancreatic microvascular structure (29).…”

Section: Discussionmentioning

confidence: 99%

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An experimental model of hemolysis-induced acute pancreatitis

Saruç

Yüceyar

Türkel

et al. 2003

Braz J Med Biol Res

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The literature indicates that acute pancreatitis is a complication of massive hemolysis with a prevalence of about 20%. We describe an experimental model of hemolysis-induced acute pancreatitis. Hemolytic anemia was induced in rats by a single ip injection of 60 mg/kg of 20 mg/ml acetylphenylhydrazine (APH) in 20% (v/v) ethanol on the first experimental day (day 0). One hundred and fifty Wistar albino rats weighing 180-200 g were divided into three groups of 50 animals each: groups 1, 2 and 3 were injected ip with APH, 20% ethanol, and physiological saline, respectively. Ten rats from each group were sacrificed on study days 1, 2, 3, 4 and 5. Serum amylase, lipase levels and pancreatic tissue tumor necrosis factor-α (TNF-α) and plateletactivating factor (PAF) contents were determined and a histological examination of the pancreas was performed. No hemolysis or pancreatitis was observed in any of the rats in groups 2 and 3. In group 1, massive hemolysis was observed in 35 (70%) of 50 rats, moderate hemolysis in seven (14%), and no hemolysis in eight (16%). Thirtythree of 35 (94.2%) rats with massive hemolysis had hyperamylasemia, and 29 of these rats (82.8%) had histologically proven pancreatitis. The most severe pancreatitis occurred on day 3, as demonstrated by histology. Tissue TNF-α and PAF levels were statistically higher in group 1 than in groups 2 and 3. Acute massive hemolysis induced acute pancreatitis, as indicated by histology, in almost 80% of cases. Hemolysis may induce acute pancreatitis by triggering the release of proinflammatory and immunoregulatory cytokines.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

An experimental model of hemolysis-induced acute pancreatitis

Saruç

Yüceyar

Türkel

et al. 2003

Braz J Med Biol Res

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“…ET-1 plays a crucial regulatory role in the microcirculation of the pancreas (Uhlmann et al 2001); it mediates not only local injury, but also systemic disease (Forgacs et al 2003). The deleterious effects of ET-1 result from its vasoactive properties and other as yet incompletely understood mechanisms, such as its influence on the release of pro-inflammatory cytokines by monocytes.…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, the most important cause of early graft pancreatitis is ischemia/reperfusion (I/R)-related disturbance of microvascular perfusion with subsequent hypoxic tissue damage. An imbalance of endothelium-derived vasoconstricting and vasodilating mediators is known to be an important contributor (Uhlmann et al 2001). The nature of leucocyte-endothelium interaction as an early step in the inflammatory response has been characterized in experimental pancreas transplantation and in models of I/R-induced acute pancreatitis (Mayer et al 1999;von Dobschuetz et al 2004).…”

Section: Introductionmentioning

confidence: 96%

Pathophysiological role of platelets in acute experimental pancreatitis: influence of endothelin A receptor blockade

et al. 2006

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The potential pathophysiological role of platelet-endothelium interactions was investigated during ischemia/reperfusion (I/R), and the effect of a selective endothelin(A) receptor antagonist (ET(A)-RA) was evaluated in an acute pancreatitis model. Acute pancreatitis was induced by warm ischemia (60 min) in Wistar rats, and its effects with and without antagonist treatment were investigated. Equivalent sham-operated animals were also studied. Microcirculatory changes were assessed by in vivo microscopy, and serum levels for lipase/amylase and histological specimens were investigated. Capillary constriction to 83.7 +/- 6.7% of sham-operated diameters was observed after 60 min of ischemia. A capillary density of 56.8 +/- 9.3% of the sham-operated group (396.3 +/- 15.8 mm(-1)) was measured after reperfusion. Stagnant leukocytes (329.5 +/- 30.4%) and platelets (337.5 +/- 32.3%) increased in postcapillary venules (P < 0.05). Administration of the ET(A)-RA significantly reduced I/R injury. Capillary diameters were maintained (101.4 +/- 4.5%), and capillary density was improved to 73.3 +/- 7.6% of sham-operated animals (P < 0.05). Stagnant leukocytes (152.3 +/- 10.6%) and platelets (207.1 +/- 19.8%) in sinusoids and postcapillary venules were reduced (P < 0.05). The extent of acute pancreatitis was reduced in the therapy group as indicated by serum lipase/amylase values and histological tissue damage (P < 0.05). Thus, ET(A)-RA therapy was effective in reducing I/R-induced pancreatitis in this experimental model.

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“…This vascular organization should be kept in mind when interpreting the islet blood-flow measurements performed with microspheres in the present study. A prerequisite for using this technique is that all microspheres became entrapped during their first passage through microvessels (34). This means that in serially connected capillary networks all microspheres were extracted in the first capillary system, and that none should pass into the second.…”

Section: Discussionmentioning

confidence: 99%

Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion

Jansson¹,

Bodin²,

Källskog³

et al. 2005

eur j endocrinol

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Objectives: The aim of this study was to evaluate islet blood-flow changes during stimulated growth of the islet organ without any associated functional impairment of islet function. Design: A duct ligation encompassing the distal two-thirds of the pancreas was performed in adult, male Sprague -Dawley rats. Methods: Pancreatic islet blood flow was measured in duct-ligated and sham-operated rats 1, 2 or 4 weeks after surgery. In some animals studied 4 weeks after surgery, islet blood flow was also measured also during hyperglycaemic conditions. Results: A marked atrophy of the exocrine pancreas was seen in all duct-ligated rats. Blood glucose and serum insulin concentrations were normal. An increased islet mass was only seen 4 weeks after surgery. No differences in islet blood perfusion were noted at any time point after duct ligation. In both sham-operated and duct-ligated rats islet blood flow was increased during hyperglycaemia; the response was, however, slightly more pronounced in the duct-ligated part of the gland. Conclusions: Normal, physiological islet growth does not cause any major changes in the islet blood perfusion or its regulation. This is in contrast to findings during increased functional demands on the islets or during deteriorated islet function, when increased islet blood flow is consistently seen. European Journal of Endocrinology 153 345-351

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Importance of Microcirculatory Disturbances in the Pathogenesis of Pancreatitis

Cited by 26 publications

References 58 publications

An experimental model of hemolysis-induced acute pancreatitis

An experimental model of hemolysis-induced acute pancreatitis

Pathophysiological role of platelets in acute experimental pancreatitis: influence of endothelin A receptor blockade

Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion

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