In order to clarify the pathogenesis of gastric mucosal lesions in patients with liver cirrhosis (LC), gastric mucosal blood flow (BF), potential difference (PD) and prostaglandin E₂ (PGE₂) of patients with LC were analyzed.
Of 277 patients with LC, gastric ulcer or gastric erosions were observed in 178 patients (64.2%). The incidence of gastric mucosal lesions in patients with LC correlated with the degree of liver damage estmated by Child's classification. BF, PD and PGE₂ in patients with LC were lower than in control patients without liver disease. BF and PD decreased as the liver damage progressed.
These results support the view that the impairment of the defensive factors of gastric mucosa represented by BF and PD play an important role in the pathogenesis of gastric mucosal lesions in patients with LC. PGE₂ was also implicated to be related to the pathogenesis of such lesions.

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Gastric mucosal lesions such as gastric ulcers and erosions are frequently observed in patients with liver cirrhosis. Although portal hypertension is suggested to play a role in the development of gastric mucosal lesions, the pathogenesis still remains undisclosed.
Gastric mucosal blood flow (BF), potential difference (PD) and prostaglandin E₂ (PGE₂) were analyzed using both rats with liver injury induced by carbon tetraoxide and rats with portal hypertension induced by incomplete portal occlusion. BF, PD and PGE₂ were lower in the rats with injured liver and with portal hypertension than in control rats. BF and PD were lower in the rats with injured liver than in the rats with portal hypertension.
These results support the view that the impairment of the defensive factors of gastric mucosa represented by BF, PD and PGE₂ play an important role in the pathogenesis of gastric mucosal lesions in rats with injured liver. Portal hypertension was considered to be a factor contributing to the impairment of the defensive factors of gastric mucosa.

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　われわれは,特異な形態を呈した食道mucosal bridge(以下食道MB)の1例を経験したので報告する.症例は,77歳男性.貧血精査のために上部消化管造影検査を施行したところMB様の病変が中部食道に認められた.それは,食道内視鏡検査によって上門歯から約25cmの中部食道に存在する食道MBと診断された.また,組織学的検索によるとそれは正常の扁平上皮に覆われていることが示唆された.　その形状は,直視内視鏡では瘻孔をともなった片側性食道狭窄様を呈し,側視内視鏡では幅広い帯状(約15mm)を呈していた.そして食道X線および内視鏡検査では.MBは気管分岐部の中部食道に存在し,それ自体が収縮するが如くにその形状は変化し,さらにMBとその周辺の背景粘膜は内視鏡的には正常の食道粘膜であった.これらの所見が現在までの後天性食道MBの報告の形態的特徴とは大きく異なっていたことから本例が先天性食道MBである可能性が考えられた.　著者らが集計し得た食道MBの本邦報告例は自験例を含めわずか38例に過ぎず,これら本邦報告例を分析し,検討を加え報告する.

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The mechanism of the hypocholesterolemic action of ursodesoxycholic acid (α-3, β-7-dihydroxycholanic acid) that were used as choleretic is not yet understood clearly. In an atempt to throw some light on the mechanism of this hypocholesterolemic action, studies were made on the incorporation of acetate-1-¹⁴C or mevalonic acid-2-¹⁴C and the fecal excretion of choleserol endproducts originating from mevalonic acid-2-¹⁴C. Male mice were used throughout the study and were placed on a cholesterol-free diet for 2 week observation period.
1. Biosynthesis:
Ten mice remained on the cholesterol-free diet and another ten mice were fed by supplementing the cholesterol-free diet with 0.5% ursodesoxycholic acid for 10 day. At the end of experimental period, one hour before killing the mice, the animals were injected with 5μc of acetate-1-¹⁴C or 0.12μc of mevalonic acid-2-¹⁴C per 20gm of body weight. The livers were excised and the incorporation into total lipid, cholesterol, fatty acid, protein and glycogen were measured. Ursodesoxycholic acid inhibited the incorporation of acetate-1-¹⁴C into total lipid, cholesterol and fatty acids and stimulated the incoration into protein and glycogen. The incoporation of mevalonic acid-2-¹⁴C into total lipid and cholesterol were inhibited, while the incorporation into protein remained unaltered. Ursodesoxycholic acid resulted in depression of the serum and hepatic chole. sterol level and elevation of hepatic glycogen and liver weight.
The present data indicate that the locus of the effect of ursodesoxycholic acid on a rate-controlling step in cholesterol biosynthesis appears to lie some-where between me valonic acid and cholesterol and between acetate and mevalonic acid.
2. Fecal excretion:
One hour after the single injection of mevalonic acid-2-¹⁴C, animals were fed a cholesterol free diet containing 0.5% ursodesoxycholic acid for 7 days. The feces collected duaring 7 days were extracted with hot ethanol and this extracts were analysed for bile acid and sterol by the technique of Mosbach et al. The total-¹⁴C activity (ethanol extract), the total sterol-¹⁴C activity and the total bile acid-¹⁴C activity were measured. Ursodesoxycholic acid greatly increased total-¹⁴C activity excretion, the stimulation occuring in the total sterol-¹⁴C activity, while excretion of the bile acid-¹⁴C activity wa deppresed.
It is concluded that the serum cholesterol-lowering effect of ursodesoxycholic acid appers to be due mainly to the inhibition of hepatic cholesterol bisoynthesis and the increase of fecal excretion of sterols.

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