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有报道,在胆盐诱发的急性胰腺炎早期,胰腺动脉收缩导致了胰腺微循环障碍。本实验的目的就是验证上述发现是否正确。胆胰管内注射牛黄脱氧胆酸钠诱发大鼠和犬胰腺炎;使用活体显微镜观察大鼠胰腺微动脉管径的变化;记录犬胰腺小动脉压的变化;计数机能毛细血管并乘以胰腺湿重校正;用激光多普勒测量胰腺灌流量。我们发现,在诱发胰腺炎后20min内大鼠胰腺微动脉扩张;犬胰腺动脉压从104.5±4.8mmHg降到54.6±5.6mmHg;5min时下腔静脉血的血细胞压积显著低于门静脉血;校正了的胰腺机能毛细血管密度增加。胰腺微循环障碍与门静脉压升高(最多升高9.18±0.78mmHg)同时发生。将门静脉压降低至基础水平可使胰腺灌流量增加约2.4倍。实验显示,在胆盐诱发急性胰腺炎的早期,胰腺动脉发生了扩张而不是收缩;这时门静脉压升高;门静脉压升高大大减小了胰腺血管压差,并导致血浆丢失和局部血液浓缩,导致胰腺微循环障碍。
It has been reported in the early bile salt-induced acute pancreatitis, pancreatic artery contraction leads to pancreatic microcirculation. The purpose of this experiment is to verify that the above findings are correct. Pancreatic duct injection of sodium bezoar deoxycholate induced pancreatitis in rats and canines; observation of the changes of the arteriolar diameter of the pancreas in rats using live microscopy; recording of arteriolar arterial pressure changes in canines; counting of functional capillaries and multiplication by pancreatic wet weight Calibration; Laser Doppler measurement of pancreatic perfusion. We found that the pancreatic micro-arteries dilated within 20 min after the induction of pancreatitis; the canine arterial pressure decreased from 104.5 ± 4.8 mmHg to 54.6 ± 5.6 mmHg; the hematocrit of the IVC was significantly lower than that of the portal vein at 5 min; Increased capillary density in pancreatic function. Pancreatic microcirculation disorders coincided with elevated portal pressure (up to 9.18 ± 0.78 mm Hg). Reducing portal pressure to basal levels increased pancreatic perfusion by approximately 2.4-fold. Experiments have shown that in the early stage of bile salt-induced acute pancreatitis, the pancreatic artery expands rather than contracts; at this time the portal pressure rises; the increase in portal pressure significantly reduces pancreatic vascular pressure and leads to loss of plasma and localized blood concentration , Leading to pancreatic microcirculation disorders.