Foitzik T, Hotz H G, Schmidt J, Klar E, Warshaw A L, Buhr H J
Department of Surgery, Klinikum Benjamin Franklin, Free University of Berlin, Germany.
Dig Dis Sci. 1995 Oct;40(10):2184-8. doi: 10.1007/BF02209003.
Extraintestinal trypsinogen activation peptides (TAP) have been shown to correlate with severity of acute pancreatitis in humans as well as in various animal models. Ischemia superimposed on experimental pancreatitis, however, increases acinar cell injury without increasing TAP in plasma. We speculated that TAP generated in the pancreas might not reach the circulation in necrotizing pancreatitis due to decreased pancreatic perfusion. To test the hypothesis that generation of TAP in plasma is related to pancreatic perfusion and that plasma TAP may therefore underestimate acinar cell injury in necrotizing disease, we correlated TAP in pancreatic tissue and body fluids with capillary pancreatic blood flow in necrotizing and edematous pancreatitis. The ratio between necrosis and TAP in tissue was similar in both models; the ratio between TAP in plasma and tissue, however, was significantly lower in necrotizing pancreatitis, indicating that a certain amount of TAP generated in the pancreas did not reach the circulation. Decreased pancreatic perfusion found in necrotizing pancreatitis was consistent with this finding. Our data suggest that TAP in tissue is most reliable to indicate severity of acute pancreatitis, whereas plasma TAP may underestimate pancreatic injury in necrotizing disease due to decreased pancreatic perfusion.
肠外胰蛋白酶原激活肽(TAP)已被证明在人类以及各种动物模型中都与急性胰腺炎的严重程度相关。然而,叠加在实验性胰腺炎上的缺血会增加腺泡细胞损伤,但不会增加血浆中的TAP。我们推测,在坏死性胰腺炎中,由于胰腺灌注减少,胰腺中产生的TAP可能无法进入循环。为了验证血浆中TAP的产生与胰腺灌注有关,因此血浆TAP可能低估坏死性疾病中腺泡细胞损伤的这一假设,我们将坏死性胰腺炎和水肿性胰腺炎中胰腺组织和体液中的TAP与胰腺毛细血管血流量进行了关联。在两种模型中,组织坏死与TAP的比率相似;然而,坏死性胰腺炎中血浆与组织中TAP的比率显著更低,这表明胰腺中产生的一定量TAP没有进入循环。坏死性胰腺炎中发现的胰腺灌注减少与这一发现一致。我们的数据表明,组织中的TAP最能可靠地指示急性胰腺炎的严重程度,而由于胰腺灌注减少,血浆TAP可能会低估坏死性疾病中的胰腺损伤。