Mukhopadhyay A K, Weisbrodt N W
Gastroenterology. 1975 Mar;68(3):444-7.
The purpose of this investigation was 2-fold: first, to determine the velocity of peristalsis in the smooth muscle area of opossum esophagus before and after administration of atropine; second, to evaluate the role of the vagus nerves in the control of the propagative nature of esophageal peristalsis. Intraluminal pressures were measured through a pressure transducer recorder system attached to continuously perfused catheters. The velocity of peristalsis in the lower third of the esophagus progressively decreased from 3.25 plus or minus 0.20 (SE) cm per sec at the 70 to 80% level to 2.17 plus or minus 0.14 (SE) at the 80 to 90%level to 1.83 plus or minus 0.10 (SE) at the 90 to 100% level. After administration of intraperitoneal atropine (100 mug per kg), the velocities were 3.1 plus or minus 0.26 (SE) cm per sec, 2.38 plus or minus 0.22 (SE), and 1.74 plus or minus 0.10 (SE), respectively, at the 70 to 80%, 80 to 90%, and 90 to 100% levels. The changes were not statistically significant. Electrical stimulation of the distal cut end of the vagus nerve induced peristaltic contractions. The velocities of peristalsis after electrical stimulation of the vagus nerve were 3.24 plus or minus 0.72 (SE) cm per sec, 2.81 plus or minus 0.64 (SE), and 1.84 plus or minus 0.34 (SE), respectively, at the 70 to 80%, 80 to 90%, and 90 to 100% levels. Results of this study indicate that the velocity of peristalsis in the smooth muscle area of the opossum esophagus has a caudally decreasing gradient. Bilateral cervical vagotomy and stimulation of the distal cut end initiates peristaltic contraction indicating that the propagative nature of peristalsis in the smooth musurrent, does not alter mucosal cyclic AMP. Dibutyryl cyclic AMP decreased net sodium absorption and increased short circuit current; findings which were qualitatively identical to those produced by taurochenodeoxycholic acid. These studies support the proposal that bile salts stimulate colonic electrolyte secretion by increasing mucosal cyclic AMP.
第一，测定阿托品给药前后负鼠食管平滑肌区域的蠕动速度；第二，评估迷走神经在控制食管蠕动传导特性中的作用。通过连接到连续灌注导管的压力传感器记录系统测量腔内压力。食管下三分之一处的蠕动速度从70%至80%水平时的每秒3.25±0.20（标准误）厘米逐渐降至80%至90%水平时的每秒2.17±0.14（标准误），再降至90%至100%水平时的每秒1.83±0.10（标准误）。腹腔注射阿托品（每千克100微克）后，在70%至80%、80%至90%和90%至100%水平时的速度分别为每秒3.1±0.26（标准误）厘米、每秒2.38±0.22（标准误）和每秒1.74±0.10（标准误）。这些变化无统计学意义。对迷走神经远端切断端进行电刺激可诱发蠕动收缩。在70%至80%、80%至90%和90%至100%水平时，迷走神经电刺激后的蠕动速度分别为每秒3.24±0.72（标准误）厘米、每秒2.81±0.64（标准误）和每秒1.84±0.34（标准误）。本研究结果表明，负鼠食管平滑肌区域的蠕动速度呈尾端递减梯度。双侧颈迷走神经切断术和对远端切断端的刺激可引发蠕动收缩，这表明平滑肌中蠕动的传导特性不受影响，不会改变黏膜环磷酸腺苷。二丁酰环磷酸腺苷降低了钠的净吸收并增加了短路电流；这些发现与牛磺鹅去氧胆酸产生的结果在性质上相同。这些研究支持了胆汁盐通过增加黏膜环磷酸腺苷来刺激结肠电解质分泌的观点。
