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出 处:《中华实验外科杂志》1998年第5期396-398,共3页Chinese Journal of Experimental Surgery
基 金:云南省应用基础研究基金
摘 要:目的探讨急性胰腺炎的发病机制。方法复制大鼠胰腺炎模型,分别经腹主动脉及外周静脉灌注改善微循环药物,观察胰腺等脏器的微循环和病理改变,以及血浆血栓素A_2及前列环素的浓度变化。结果腹主动脉灌注较外周静脉灌注微循环改善显著,血栓素浓度明显降低(P<0.01),病理改变明显好转。结论胰腺等脏器的微循环障碍与血栓素A_2的产生互为因果,二者既是重症胰腺炎的始动因素,又是恶化因素。早期经腹主动脉灌注改善微循环药物可防止重症胰腺炎发展。To study the of pathogenesis of severe acute pancreatitis (SAP). Methods Minic models of rats with SAP were replicated. Retrograde injection of 3.5% sodium traurodeoxideocholic acid into them via pancreatic-bile duct with the catheters to abdominal aorta and peripheral blood vessel was performed. Then the concentrations of plasmic TXA_2 and PGI_2 were measured by RIA. The changes of pancreatic morphology were observed by macroscopy and microscopy, and microcirculation observed by intravital microscopy too. Results The concentration of plasmic TXA_2 is rapidly decreased in abdominal aorta perfusion. With the difference in the changes of pancreatic morphology and microcirculation and the concentration of plasmic TXA_2 being significant (P<0.01). Conclusions The obstade of pancreatic microcirculation is the cause and effect of the prodrction of TXA_2. Both make SAP start and worsen. The early use of drug of improving microcirculation by abdominal aorta perfusion can prevent SAP from worsening.
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