Impact of microcirculatory flow pattern changes on the development of acute edematous and necrotizing pancreatitis in rabbit pancreas

• Verfasst von: Klar, Ernst [VerfasserIn]
• Verfasst von: Schratt, W. [VerfasserIn]
• Verfasst von: Foitzik, Thomas [VerfasserIn]
• Verfasst von: Buhr, Heinz J. [VerfasserIn]
• Verfasst von: Herfarth, Christian [VerfasserIn]
• Verfasst von: Messmer, K. [VerfasserIn]
• Titel: Impact of microcirculatory flow pattern changes on the development of acute edematous and necrotizing pancreatitis in rabbit pancreas
• Verf.angabe: E. Klar, W. Schratt, T. Foitzik, H. Buhr, C. Herfarth, K. Messmer
• E-Jahr: 1994
• Jahr: December 1994
• Umfang: 6 S.
• Fussnoten: Gesehen am 03.07.2024
• Titel Quelle: Enthalten in: Digestive diseases and sciences
• Ort Quelle: Dordrecht : Springer Science + Business Media B.V., 1934
• Jahr Quelle: 1994
• Band/Heft Quelle: 39(1994), 12, Seite 2639-2644
• ISSN Quelle: 1573-2568
• DOI: doi:10.1007/BF02087702
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: acute pancreatitis
• Sach-SW: edema
• Sach-SW: microcirculation
• Sach-SW: necrosis
• Sach-SW: pathogenesis
• Sach-SW: permeability
• K10plus-PPN: 1893791785

Abstract

Impairment of pancreatic microcirculation has often been advocated as one pathogenic mechanism in necrotizing pancreatitis. In contrast, data on pancreatic capillary perfusion in edematous pancreatitis are scarce. It was the aim of this experimental study to compare changes in pancreatic microcirculation in edematous and necrotizing pancreatitis. Twelve rabbits were allocated to two groups. Two different models of acute pancreatitis were used. Edematous pancreatitis was elicited by intravenous administration of cerulein (25 µg/kg/hr) (N=6). Necrotizing pancreatitis of the biliary type was induced by pressure-controlled intraductal infusion of a mixture of taurocholate, trypsin, and blood (N=6). Pancreatic microcirculation was quantified by means of intravital microscopy assessing functional capillary density, blood cell velocity, and distribution of the plasma marker FITC-dextran 70. Systemic hemodynamics were maintained at baseline values by fluid administration. Regardless of edema or necrosis, pronounced extravasation of FITC-dextran was recorded in the early stage of pancreatitis. In cerulein-induced pancreatitis, hyperemia developed as indicated by an increase in blood cell velocity in the presence of homogeneous capillary perfusion. In contrast, a progressive reduction of the number of perfused capillaries was detected in necrotizing pancreatitis. In conclusion, pancreatic microvascular perfusion may be regarded as an important pathogenetic factor for the determination of acute pancreatitis.