Intestinal microcirculation and gut permeability in acute pancreatitis: Early changes and therapeutic implications |
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Authors: | Dr Hubert G Hotz MD Thomas Foitzik MD Janine Rohweder MD Joerg D Schulzke MD Micbael Fromm MD Norbert S F Runkel MD Heinz J Bubr MD EACS |
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Institution: | 1. Department of Surgery, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany.;2. Department of Gastroenterology, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany.;3. Department of Clinical Physiology, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin, Germany. |
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Abstract: | Translocation of bacteria from the intestine causes local and systemic infection in severe acute pancreatitis. Increased intestinal
permeability is considered a promoter of bacterial translocation. The mechanism leading to increased gut permeability may
involve impaired intestinal capillary blood flow. The aim of this study was to evaluate and correlate early changes in capillary
blood flow and permeability of the colon in acute rodent pancreatitis of graded severity. Edematous pancreatitis was induced
by intravenous cerulein; necrotizing pancreatitis by intravenous cerulein and intraductal glycodeoxycholic acid. Six hours
after induction of pancreatitis, the permeability of the ascending colon was assessed by the Ussing chamber technique; capillary
perfusion of the pancreas and colon (mucosal and subserosal) was determined by intravital microscopy. In mild pancreatitis,
pancreatic capillary perfusion remained unchanged (2.13 ± 0.06 vs. 1.98 ± 0.04 nl-min−l.cap −1 control]; P = NS), whereas mucosal (1.59 _± 0.03 vs. 2.28 ± 0.03 nl.min−l.cap −1 control]; P <0.01) and subserosal (2.47 ± 0.04 vs. 3.74 ± 0.05 nl-min−l.cap -1 control]; P <0.01) colonic capillary blood flow was significantly reduced. Severe pancreatitis was associated with a marked
reduction in both pancreatic (1.06 = 0.03 vs. 1.98 ± 0.04 nl’min-1.cap -1 control]; P <0.01) and colonic (mucosal: 0.59 = 0.01 vs. 2.28 ± 0.03 nl.min−l.cap -1 control], P < 0.01; subserosal: 1.96 ± 0.05 vs. 3.74 ± 0.05 nl.min−l.cap -1 control], P <0.01) capillary perfusion. Colon permeability tended to increase with the severity of the disease (control:
147 ±19 nmol.hr−l.cm {−2}2; mild pancreatitis: 158±23 nmol-hr−l.cm-2; severe pancreatitis: 181 ±33 nmol.hr−l.cm-2; P = NS). Impairment of colonic capillary perfusion correlates with the severity of pancreatitis. A decrease in capillary blood
flow in the colon, even in mild pancreatitis not associated with significant protease activation and acinar cell necrosis
or impairment of pancreatic capillary perfusion, suggests that colonic microcirculation is especially susceptible to inflammatory
injury. There was no significant change in intestinal permeability in the early stage of pancreatitis, suggesting a window
of opportunity for therapeutic interventions to prevent the later-observed increase in gut permeability, which could result
in improved intestinal microcirculation.
Presented at the Thirty-Seventh Annual Meeting of The Society for Surgery of the Alimentary Tract, San Diego, Calif., May
19–22, 1996.
Supported in part by Deutsche Forschungsgemeinschaft (DFG Fo 197/3). |
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Keywords: | Acute pancreatifis colon microcirculation permeability bacterial translocation |
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