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目的证实应激过程中胆汁反流的存在,探讨胆囊收缩素八肽(CCK-8)在应激所致胆汁反流中的作用及相关机制。方法放免法检测大鼠血浆 CCK-8和胃液胆汁酸水平,测定胃液 pH值并记录胃黏膜溃疡指数;多导生理记录仪记录离体肌条收缩活动;检测 Fura-2/AM 标记的胃窦平滑肌细胞(SMC)内钙离子浓度([Ca~(2+)]i)的变化;全细胞膜片钳记录 L-型钙通道电流(I_(Ca-L))。结果与正常对照相比,应激时血浆 CCK-8[从(2.23±0.88)pmol/L 到(10.80±3.82)pmol/L],胃液胆汁酸[从(37.93±23.76)μmol/L 到(1316.00±197.36)μmol/L],pH 值(从1.06±1.20到5.29±1.25)和溃疡指数(从0.62±0.23到32.01±16.11)均明显增高(P<0.01);CCK-8S 显著增强胃窦和幽门肌条收缩和胃窦 SMC 的[Ca~(2+)]i[从(65.8±7.4)nmol/L 升至(472.1±35.6)nmol/L,P<0.01]及 I_(Ca-L)[从(-56.42±6.57)pA 增至(-88.54±5.71)pA,P<0.01],但可被相应拮抗剂所抑制。结论与应激时 CCK-8升高所致的胃窦动力紊乱相关,胆汁反流存在于应激过程中,是应激性胃黏膜损伤的重要因素。
Objective To confirm the existence of bile reflux during stress and to explore the role and mechanism of cholecystokinin octapeptide (CCK-8) in stress-induced bile reflux. Methods Radioimmunoassay was used to detect plasma CCK-8 and bile acid levels in gastric juice. Gastric fluid pH value was measured and gastric mucosal ulcer index was recorded. Contractile activity was recorded by multi-conductance log recorder. Fura-2 / AM labeled gastric antrum The changes of calcium ion concentration ([Ca ~ (2 +)] i) in smooth muscle cells (SMC) were recorded. L-type calcium channel current (I_ (Ca_ L)) was recorded by whole- Results Compared with the normal control group, the levels of CCK-8 in plasma (from (2.23 ± 0.88) pmol / L to (10.80 ± 3.82) pmol / L) and gastric acid bile acid (from 37.93 ± 23.76 μmol / L to (Ranging from 1.06 ± 1.20 to 5.29 ± 1.25) and ulceration index (from 0.62 ± 0.23 to 32.01 ± 16.11) (P <0.01). CCK-8S significantly increased gastric antrum (P <0.01) and I_ (Ca_ (2)) i increased from (65.8 ± 7.4) nmol / L to (472.1 ± 35.6) nmol / L in gastric antrum, ) Increased from (-56.42 ± 6.57) pA to (-88.54 ± 5.71) pA, P <0.01], but was inhibited by the corresponding antagonist. CONCLUSIONS: It is related to the disorder of gastric antrum caused by the elevation of CCK-8 during stress, and bile reflux exists in the process of stress, which is an important factor of stress gastric mucosal injury.