BACKGROUND: Graft pancreatitis is thought to be induced by ischemia/reperfusion. Animal experiments have suggested that an impaired microcirculation is crucial in this process. We have therefore studied the relevance of microcirculation in clinical pancreas transplantation. METHODS: In 17 patients undergoing pancreas transplantation, tissue pO2 was monitored continuously by an electrode implanted into the pancreatic tail. A catheter was inserted in the distal part of the splenic vein of the pancreas graft. After reperfusion blood samples were taken from this catheter and blood flow was measured by the venous outflow method. The degree of graft pancreatitis was assessed by peak-C-reactive protein (CRP) defined as highest CRP within 3 days after transplantation. RESULTS: Tissue pO2 increased within 5 min after reperfusion. Thereafter, in most patients a transient decrease was noted, indicating impairment of nutritive perfusion. During this period there was an increasing negative correlation between peak-CRP and tissue pO2 which was highly significant at 60 min after reperfusion (r=-0.70, P<0.002). Also donor age correlated significantly with peak-CRP (r=0.64, P<0.005) and to a somewhat lesser extend with tissue pO2 60 min after reperfusion (r= -0.55, P<0.03). CONCLUSION: These data show that the degree of organ damage in clinical pancreas transplantation is directly related to an impairment of microcirculation in the early reperfusion period. These data also support the idea that grafts from older donors have a higher probability to develop graft pancreatitis and that this might be due to an increased incidence of microcirculatory disturbances in these organs.
BACKGROUND: Graft pancreatitis is thought to be induced by ischemia/reperfusion. Animal experiments have suggested that an impaired microcirculation is crucial in this process. We have therefore studied the relevance of microcirculation in clinical pancreas transplantation. METHODS: In 17 patients undergoing pancreas transplantation, tissue pO2 was monitored continuously by an electrode implanted into the pancreatic tail. A catheter was inserted in the distal part of the splenic vein of the pancreas graft. After reperfusion blood samples were taken from this catheter and blood flow was measured by the venous outflow method. The degree of graft pancreatitis was assessed by peak-C-reactive protein (CRP) defined as highest CRP within 3 days after transplantation. RESULTS: Tissue pO2 increased within 5 min after reperfusion. Thereafter, in most patients a transient decrease was noted, indicating impairment of nutritive perfusion. During this period there was an increasing negative correlation between peak-CRP and tissue pO2 which was highly significant at 60 min after reperfusion (r=-0.70, P<0.002). Also donor age correlated significantly with peak-CRP (r=0.64, P<0.005) and to a somewhat lesser extend with tissue pO2 60 min after reperfusion (r= -0.55, P<0.03). CONCLUSION: These data show that the degree of organ damage in clinical pancreas transplantation is directly related to an impairment of microcirculation in the early reperfusion period. These data also support the idea that grafts from older donors have a higher probability to develop graft pancreatitis and that this might be due to an increased incidence of microcirculatory disturbances in these organs.
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