Yamana H, Yatsuka K, Kakegawa T
Gastroenterol Jpn. 1983 Apr;18(2):119-27. doi: 10.1007/BF02774686.
In spite of many attempts to produce an experimental model for studying the pathogenesis and the pathophysiology of portal hypertension and esophageal varices, satisfactory results have not been reported. Since most attempts involved multiple operations or complicated surgical maneuvers to achieve portal hypertension, experimental animals could not survive easily. This new procedure requires only a simple operation, so experimental animal survival is high. The portal venous pressure can be raised immediately by increasing intrahepatic vascular resistance. This is done by wrapping and compressing the whole liver with polypropylene mesh, which also prevents the development of hepatopetal collaterals. The experimental production of portal hypertension in fifteen dogs resulted in only one death. The remaining fourteen dogs were in good condition for nine weeks after the operation and were maintaining elevated ranges of portal pressure with an average of 326 mmH2O. Varying degrees of esophageal venous dilatation were evident. Based on the results, this newly developed method seems to be useful for studying the pathophysiology of the portal hypertension and esophageal varices.
尽管人们多次尝试建立用于研究门静脉高压症和食管静脉曲张的发病机制及病理生理学的实验模型，但尚未有令人满意的结果报道。由于大多数尝试都涉及多次手术或复杂的外科操作来实现门静脉高压，实验动物难以轻易存活。这种新方法仅需简单的手术，因此实验动物的存活率很高。通过增加肝内血管阻力可立即升高门静脉压力。这是通过用聚丙烯网包裹并压缩整个肝脏来实现的，这也可防止向肝侧支循环的形成。对15只狗进行门静脉高压的实验性造模，仅导致1只死亡。其余14只狗术后9周状况良好，门静脉压力维持在升高范围，平均为326 mmHg₂O。可见不同程度的食管静脉扩张。基于这些结果，这种新开发的方法似乎有助于研究门静脉高压症和食管静脉曲张的病理生理学。
