Yamasaki T, Chijiiwa K, Chijiiwa Y
Department of Surgery I, Kyushu University Faculty of Medicine, Fukuoka, Japan.
J Surg Res. 1995 Dec;59(6):743-6. doi: 10.1006/jsre.1995.1233.
A close relation between the hyperhormonism of somatostatin and gallstone disease suggested to us the hypothesis that somatostatin inhibits cholecystokinin (CCK)-induced gallbladder contraction on the level of target organs. To investigate this hypothesis, smooth muscle cells were isolated from human and canine gallbladders and the direct inhibitory effects of somatostatin on the CCK-induced cell contraction were examined in vitro. Somatostatin alone had no effect on the cell motility, while it significantly inhibited the cholecystokinin-octapeptide (10(-10) M)-induced cell contraction at the concentration of 10(-6) M (P < 0.01) in both human and canine gallbladders. The results demonstrate for the first time that somatostatin has a direct inhibitory action against cholecystokinin-induced gallbladder contraction. This may partly account for the high frequency of gallstone disease in patients with somatostatinoma.
生长抑素在靶器官水平上抑制胆囊收缩素（CCK）诱导的胆囊收缩。为了验证这一假说，从人和犬的胆囊中分离出平滑肌细胞，并在体外检测生长抑素对CCK诱导的细胞收缩的直接抑制作用。单独使用生长抑素对细胞运动没有影响，而在人和犬的胆囊中，它在浓度为10^(-6) M时能显著抑制胆囊收缩素八肽（10^(-10) M）诱导的细胞收缩（P < 0.01）。结果首次证明生长抑素对胆囊收缩素诱导的胆囊收缩具有直接抑制作用。这可能部分解释了生长抑素瘤患者胆结石病的高发病率。
