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目的检测氨甲酰胆碱（ＣＣｈ）对人未妊娠峡部子宫平滑肌细胞（ＣＭＣ）内游离钙离子浓度（［Ｃａ２＋］ｉ）及生物合成１，４，５三磷酸肌醇（ＩＰ３）的影响，探讨Ｍ受体激动剂升高人子宫平滑肌［Ｃａ２＋］ｉ作用与影响膜肌醇磷酯代谢的关系。方法应用荧光分光光度计检测［Ｃａ２＋］ｉ水平；应用同位素放射免疫分析法检测ＩＰ３水平。结果基础状态下ＣＭＣ［Ｃａ２＋］ｉ为（１７８±２１）ｎｍｏｌ·Ｌ－１，１、１０和１００μｍｏｌ·Ｌ－１ＣＣｈ使［Ｃａ２＋］ｉ升高分别为（２４４±３１）、（３２６±３９）和（４３７±６１）ｎｍｏｌ·Ｌ－１，呈剂量依赖性；细胞外无钙时ＣＣｈ升高［Ｃａ２＋］ｉ作用被减弱；１０μｍｏｌ·Ｌ－１阿托品（Ａｔｒ）可阻断ＣＣｈ升高［Ｃａ２＋］ｉ的作用。基础状态下ＣＭＣ内ＩＰ３水平为（８１５±８６）ｎｍｏｌ·ｇ－１Ｐｒｏ。１，１０和１００μｍｏｌ·Ｌ－１的ＣＣｈ可诱导ＩＰ３水平升高，其峰值是在ＣＣｈ孵育５ｍｉｎ时，此时升高的ＩＰ３水平分别为（１０７±１５），（１３５±３１）和（１４８±２９）ｎｍｏｌ·ｇ－１Ｐｒｏ。１０μｍｏｌ·Ｌ－１Ａｔｒ可显著抑制ＣＣｈ促ＩＰ３生成作用。结论ＣＣｈ通过激动Ｍ受体使ＣＭＣ的［Ｃ?
Objective To investigate the effect of carbachol (CCh) on intracellular free calcium concentration ([Ca2 +] i) and biosynthesis of 1,4,5-triphosphate (IP3) in human uterine isthmus uterine smooth muscle cells (CMC) To explore the role of M receptor agonist in the increase of [Ca2 +] i in human uterine smooth muscle and the relationship with the influence of membrane phospholipid metabolism. Methods The level of [Ca2 +] i was measured by fluorescence spectrophotometer. The level of IP3 was detected by radioimmunoassay. Results The basal state of [Ca2 +] i was (178 ± 21) nmol·L-1, 1, 10 and 100 μmol·L-1CCh, and the increase of [Ca2 +] i was (244 ± 31) and (326 ± 39) And (437 ± 61) nmol·L-1 in a dose-dependent manner. The effect of CCh on [Ca2 +] i was weakened when extracellular calcium was not added. Atr of 10μmol·L-1 atropine could block the increase of [Ca2 + ] I’s role. Under the basal condition, the level of IP3 in CMC was (815 ± 8.6) nmol · g-1Pro. IPh levels increased at 1, 10 and 100 μmol·L-1 CCh, and peaked at 5 min after CCh incubation. The elevated IP3 levels were (107 ± 15), (135 ± 31) and ± 29) nmol · g-1Pro. 10μmol·L-1Atr significantly inhibited CCh-induced IP3-producing effect. Conclusions CCh stimulates M receptors to make [C?