门静脉压和局部血液表观黏度在急性胰腺炎胰腺微循环障碍中的表达

Portal Vein Pressure and Local Hemoconcentration in the Development of Pancreatic Microcirculatory Disturbance in Acute Pancreatitis

目的根据Hagen-Poiseuille方程[Q=π(P1-P2)R4/8μl],胰腺血管压差(P1-P2)和胰腺血管内血液表观黏度(μ)决定胰腺的血液灌注(pancreatic blood flow,PBF,Q)。因此,本实验研究门静脉压和局部血液表观黏度在急性胰腺炎胰腺微循环障碍中的作用。方法胆胰管内注射牛黄脱氧胆酸钠诱发大鼠和犬急性胰腺炎。记录颈动脉压、门静脉压、胰腺小动脉压和肠系膜上动脉压。用激光多普勒测量大鼠胰腺十二指肠部的血液灌流量。结果在急性胰腺炎的早期,门静脉压(Pvp,P2)增高可达一倍。将门静脉压人为地保持在基础水平,可以诱发急性胰腺炎,10min后大鼠胰腺灌流量增加1.4倍。发生在胰腺内的血浆外渗造成局部血液的血细胞比容显著高于全身其他血管的血液;局部的血液浓缩导致局部的血液表观黏度显著高于他处血液。结论门静脉压升高和局部血液黏度增高是引起急性胰腺炎胰腺微循环障碍的重要机理。

Objective According to Hagen-Poiseuille equation[ Q = p（P1-P2） R4/8/μL], the pancreatic perfusion（ PBF, Q） is affected by the pressure difference along pancreatic vessels（ P1-P2） and the apparent blood viscosity within pancreas（μ）. We carried out this study to determine these variables. Methods Acute pancreatitis was induced with time-controlled intraductal infusion of taurodeoxycholate in rats and dogs. Blood pressures was recorded. Pancreatic perfusion was measured with laser Doppler flowmeter. Results Portal vein pressure（ Pvp, P2） doubled in the early phase of acute pancreatitis. Normalization of Pvp was associated with a 1.4-fold increase of pancreatic perfusion（ 10 rain after pancreatitis induction） in rats. Plasma extravasation in pancreas led to a marked difference between systemic and local hematocrits. Local hemoconcentration resulted in higher local μ compared with systemic circulation. Conclusion The rise of Pvp and local μ contributes to pancreatic microcirculatory disturbance.