Hosokawa Y
Third Department of Internal Medicine, Ehime University School of Medicine, Japan.
Gastroenterol Jpn. 1991 Jun;26(3):329-35. doi: 10.1007/BF02781921.
Gastric mucosal lesions are an inevitable complication in patients with liver cirrhosis. Their etiology, however, is as yet unknown. The present study investigated phospholipid metabolism in the gastric mucosa of rats with cirrhosis induced by carbon tetrachloride. Gastric mucosal lesions were induced by taurocholic acid (TCA) which was given through a gastric tube. Levels of phospholipids, phosphatidylcholine, and disaturated-phosphatidylcholine were found to be markedly reduced at the mucosal surface in the cirrhotic rats, and they were increased in the gastric juice. Metabolism of phospholipids in the gastric mucosa was visualized by 3H-choline autoradiography and the rate of phospholipid metabolism was found to be reduced. These results strongly suggest that mucosal lesions induced by bile regurgitation into the stomach are due to disturbance of phospholipid metabolism in the gastric mucosa.
胃黏膜病变是肝硬化患者不可避免的并发症。然而,其病因尚不清楚。本研究调查了四氯化碳诱导的肝硬化大鼠胃黏膜中的磷脂代谢。通过胃管给予牛磺胆酸(TCA)诱导胃黏膜病变。发现肝硬化大鼠黏膜表面的磷脂、磷脂酰胆碱和二饱和磷脂酰胆碱水平显著降低,而胃液中的这些物质水平升高。通过3H-胆碱放射自显影观察胃黏膜中磷脂的代谢情况,发现磷脂代谢速率降低。这些结果强烈表明,胆汁反流至胃引起的黏膜病变是由于胃黏膜中磷脂代谢紊乱所致。