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为了估计豚鼠离体胆囊和胆管肌条收缩过程中细胞内、外钙的相对关系,本实验设计在有钙或无钙的 Krebs 氏液中激动剂—ACh 或雨蛙肽刺激肌条收缩的效应,结果如下:(1)无论是在有钙还是无钙液内激动剂均引起肌条收缩,在有钙液内激动剂的作用较大。(2)在无钙液中激动剂引起的胆囊收缩将减小50～60%,P<0.001,胆管减小70.8～82.5%,P<0.001。ACh引起肌条收缩达峰值的时间显著延长,而雨蛙肽则缩短。(3)在无钙液中激动剂引起肌条最大收缩后,再加 CaCl_2,胆囊收缩可恢复到有钙水平,胆管恢复到有钙水平的40.2～62.3%。(4)在无钙液中阿托品极明显地减弱 ACh 刺激胆囊收缩的效应,补充钙后肌条收缩可以恢复。这些结果提示,激动剂刺激胆囊或胆管肌条收缩时,细胞内、外钙离子均有作用,以细胞外钙的作用较强,而胆管收缩更依赖于细胞外钙。阿托品还可能阻碍细胞内钙的释放而发挥作用。
In order to estimate the relative relationship between intracellular calcium and extracellular calcium during guinea pig gallbladder and bile duct contraction, we designed the effect of ACh or melatonin to stimulate contractions of muscle strips in Krebs’s solution with or without calcium. The results are as follows: (1) whether there is calcium or calcium-free fluid within the agonist caused muscle contraction, in calcium with a larger role of agonists. (2) Gallbladder contraction induced by agonist in calcium-free fluids would be reduced by 50-60%, P <0.001, and bile duct decrease 70.8-82.5%, P <0.001. ACh caused muscle contraction peak time significantly longer, while the phytolaccae shortened. (3) In the absence of calcium agonists cause maximum contraction of muscle strips, coupled with CaCl_2, gallbladder contraction can be restored to calcium levels, bile duct recovery to calcium levels of 40.2 to 62.3%. (4) atropine in the absence of calcium significantly reduced the ACh stimulation of gallbladder contraction effect, calcium supplementation of muscle contraction can be restored. These results suggest that agonist stimulation of gallbladder or bile duct muscle contraction, the intracellular and extracellular calcium ions have a role to the role of extracellular calcium stronger biliary contraction more dependent on extracellular calcium. Atropine may also hinder the release of intracellular calcium to play a role.