Ischemia/Reperfusion Injury of the Pancreas: A New Animal Model

Benz, Stefan; Schnabel, Ralf; Morgenroth, K; Weber, Heike; Pfeffer, F.; Hopt, Ulrich T.

doi:10.1006/jsre.1998.5269

Cited by 42 publications

(26 citation statements)

References 13 publications

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“…Perfusion failure in microvascular systems may be due to leukocyte adhesion and infiltration (25), intravascular hemoconcentration (26), higher microvascular resistance (tissue edema and endothelial swelling) (11,27), derangement of coagulation (2) and vasoconstriction due to a massive systemic increase of catecholamines (28). All these mechanisms, previously described in BD experiments on other organs, may also be relevant to the pancreas.…”

Section: Discussionmentioning

confidence: 96%

Brain Death Impairs Pancreatic Microcirculation

Obermaier

Dobschuetz

Keck

et al. 2004

American Journal of Transplantation

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Brain death (BD) influences the quality of donor grafts in transplantation. To evaluate the impact of BD on pancreas grafts, we investigated the influence of BD on the microcirculation and histology of the pancreas in a rat model of explosive BD. A group of Wistar rats (n = = 7), rendered brain dead by inflating an intracranially inserted Fogarty catheter was compared with controls (CO) using intravital epifluorescence-microscopy over 4 h after BD induction; functional capillary density (FCD), leukocyte adherence (AL) in post-capillary venules, histology and pancreatic enzymes were investigated. Four hours after BD, FCD decreased (333 ± 11 vs. baseline 444 cm/cm 2 ± 5 SEM; p < 0.01) and showed lower values than CO (388 ± 9 p < 0.01). In BD, AL was increased (628 cells/mm 2 ± 110 SEM vs. baseline 123 ± 32, and vs. CO 180 ± 33; p < 0.001). BD caused increased histological damage (CO 1.6 scorepoints ± 0.7 SD vs. BD 8.3 ± 7.1; p < 0.05). Amylase was higher in BD (p < 0.05) but did not reach pathological values. We show for the first time that BD causes relevant changes in pancreatic microcirculation, histology and leukocyte endothelial interaction which might have a serious impact on the function of grafts. New strategies for preventing this damage are therefore highly desirable in order to improve the outcome of pancreas transplantation.

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Section: Discussionmentioning

confidence: 96%

Brain Death Impairs Pancreatic Microcirculation

Obermaier

Dobschuetz

Keck

et al. 2004

American Journal of Transplantation

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“…Different animal models have greatly expanded the understanding of pancreatic microcirculation physiology and the downstream cellular and microvascular consequences, evolving in response to pancreas transplantation (2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Attempts to visualize the human pancreatic microcirculation using intra-vital microscopy have been limited mainly due the large size of the intra-vital microscopic set-up, the requirement of toxic fluorescence dyes for plasma contrast enhancement and the development of dye-associated phototoxic effects (12).…”

Section: Introductionmentioning

confidence: 99%

In Vivo Imaging of Human Pancreatic Microcirculation and Pancreatic Tissue Injury in Clinical Pancreas Transplantation

Schaser

Puhl

Vollmar

et al. 2005

American Journal of Transplantation

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Pancreatitis remains to be a major complication following clinical pancreas transplantation. We performed orthogonal polarized spectral (OPS) imaging for direct in vivo visualization and quantification of human pancreatic microcirculation in six healthy donors for living donor liver transplantation and 13 patients undergoing simultaneous pancreas-kidney transplantation. We further determined the impact of microvascular dysfunction during early reperfusion on pancreatic graft injury. Exocrine and endocrine pancreatic impairment was determined by analysis of serum lipase, amylase and C-peptide levels. Compared to normal pancreas in liver donors (homogeneous acinar perfusion) functional capillary density (FCD) and capillary red blood flow velocity of reperfused grafts were significantly decreased. Elevated CRP concentrations on day 2 post-transplant and serum lipase and amylase levels determined on days 4-5 significantly correlated with microvascular dysfunction during the first 30 min of graft reperfusion. Post-transplant serum C-peptide also correlated significantly with pancreatic capillary perfusion. OPS imaging allows to intra-operatively assess physiologic pancreatic microcirculation and to determine microcirculatory impairment during early graft reperfusion. This impairment correlated with the manifestation of post-transplant dysfunction of both exocrine and endocrine pancreatic tissue. OPS imaging may be used clinically to determine the efficacy of interventions, aiming at attenuating microcirculatory impairment during the acute post-transplant reperfusion phase.

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“…Furthermore, clinical and experimental findings have shown the relevance of pancreatic ischemia/reperfusion injury. Reduced pancreas perfusion, as for example during shock, acute or chronic pancreatitis, and completely interrupted blood supply after pancreas transplantation, can trigger pancreatitis and also may have an important influence on its severity [3][4][5][6][7]. Graft pancreatitis after pancreas transplantation can be considered a human model of pancreatic ischemia/reperfusion.…”

Section: Introductionmentioning

confidence: 99%

Ischemia/reperfusion-induced pancreatitis in rats: a new model of complete normothermic in situ ischemia of a pancreatic tail-segment

et al. 2001

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Ischemia/reperfusion injury plays an important role in the development of graft pancreatitis and thrombosis after pancreas transplantation. Up to now there are few therapeutic options for this severe complication because very little is known about pancreatic ischemia/reperfusion injury. The same pathomechanisms may also be involved in the induction and determination of the course of acute pancreatitis. We observed the effect of 2 h of warm in situ ischemia on the postischemic tissue oxygenation, histological organ damage, and pancreatic enzymes. Experiments were performed in 21 male Wistar rats. In sham-operated animals without ischemia, the pancreas was not dissected. In the ischemia/reperfusion group a pancreatic tail-segment was carefully separated from the head, and ischemia was induced by clamping the splenic vessels for 2 h, after flushing the pancreatic tail-segment with heparinized saline. Animals treated similarly, but with opening of the clamps some seconds after induction of ischemia, served as controls. The animals were observed for 2 h after reperfusion. Tissue oxygenation was monitored by a PO2-sensitive probe (LICOX, GMS, Kiel, Germany) which was implanted into the pancreatic tissue. Blood samples were taken before, 5 min, 60 min, and 120 min after reperfusion. At the end of the experiment the pancreatic tail was excised for histological examination; biopsies froin the non-ischemic pancreatic head served as intraindividual control to exclude side effects on the nonischemic pancreatic head. In the ischemia/reperfusion group, PO2ti was significantly lower 1 h (18.0+/-1.7 mmHg) and 2 h (16.4+/-1.6 mmHg) after reperfusion compared with baseline conditions (32.8+/-5.2 mmHg) and the control group (1 h 30.6+/-1.9 mmHg, 2 h 32.4+/-2.4 mmHg). Histological injury score and plasma lipase activity were significantly higher in the ischemia/reperfusion group compared with the control group. Thus we describe a new experimental model of complete normothermic in situ ischemia of a pancreatic tail-segment with the possibility of flushing the pancreatic tail-segment and selective local application of drugs to the pancreas.

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Ischemia/Reperfusion Injury of the Pancreas: A New Animal Model

Cited by 42 publications

References 13 publications

Brain Death Impairs Pancreatic Microcirculation

Brain Death Impairs Pancreatic Microcirculation

In Vivo Imaging of Human Pancreatic Microcirculation and Pancreatic Tissue Injury in Clinical Pancreas Transplantation

Ischemia/reperfusion-induced pancreatitis in rats: a new model of complete normothermic in situ ischemia of a pancreatic tail-segment

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