Exocrine, but not endocrine, tissue is susceptible to microvascular ischemia/reperfusion injury following pancreas transplantation in the rat.

While post-transplant pancreatitis is still a frequently occurring complication of whole pancreas transplantation, dysfunction of the endocrine tissue is rarely observed. Given that microcirculatory disorders play a major role in the pathogenesis of pancreatitis, we hypothesized a dissociation of endocrine and exocrine microvascular control in pancreas transplantation (cold ischemia-reperfusion) and studied this dissociation quantitatively, analyzing the pancreatic microcirculation after heterotopic isogeneic pancreaticoduodenal transplantation in rats by means of fluorescence microscopy. Functional capillary density (FCD) of both exocrine and endocrine tissue of pancreatic grafts after 1 h of cold storage in HTK solution did not differ when compared to sham-operated, time-matched controls. Intermittent capillary perfusion, which is absent under sham control conditions and which is proposed to be operative as a compensatory mechanism to counteract malperfusion, was observed in 52% of the exocrine, but in only 8% of the endocrine, tissue studied (p < 0.05). In contrast, cold storage of pancreatic grafts for 6 h in HTK resulted in a complete loss of intermittent capillary perfusion in exocrine tissue and, consequently, marked exocrine perfusion failure (decrease in FCD), while FCD of pancreatic endocrine tissue was preserved without any significant change in the incidence of intermittent capillary perfusion. Thus, our results indicate a higher susceptibility of the exocrine pancreas to cold ischemia/reperfusion events that is associated with significant alterations in nutritive perfusion and, thus, with limitations of the oxygen supply to the tissue. This may lead to inflammatory tissue reactions in the clinical setting of pancreas transplantation.