Ren J L, Dodds W J, Martin C J, Dantas R O, Mittal R K, Harrington S S, Kern M K, Brasseur J G
Department of Radiology, Medical College of Wisconsin, Milwaukee 53226.
Am J Physiol. 1991 Sep;261(3 Pt 1):G417-25. doi: 10.1152/ajpgi.1991.261.3.G417.
Our aim in this study was to determine the effect of variations in intrabolus pressure on esophageal peristalsis. In five cats, intrabolus pressure was altered by increasing intragastric pressure to 20-45 mmHg by use of a pressure cuff to compress the abdomen. In each cat, increases in intragastric pressure were associated with comparable increases in pressure of the esophageal bolus while the bolus was in the distal esophagus during esophageal peristalsis. Secondary peristalsis induced by a 5-ml injection of barium into the proximal esophagus was recorded by synchronized videofluoroscopy and esophageal manometry. Graded increases in intrabolus pressure caused an increased prevalence of ineffective, incomplete peristaltic sequences that did not completely clear barium from the esophagus. At intragastric pressures greater than 45 mmHg, 63% of the peristaltic sequences were incomplete. Increases in intrabolus pressure elicited by increased intragastric pressure also caused 1) slowing of the peristaltic wave in the distal esophagus, 2) increased pressure wave duration in the distal esophagus, 3) increased esophageal diameter, and 4) increased duration of lower esophageal sphincter opening. The incidence of retrograde bolus escape was inversely related to the difference between peristaltic wave amplitude and intrabolus pressure. A pressure difference of greater than 20 mmHg prevented retrograde barium escape at all esophageal levels, whereas a difference of less than 20 mmHg was generally associated with retrograde escape of barium in the distal esophagus. We conclude that an increase in intrabolus pressure causes an increase in esophageal distension that is transduced into alterations of esophageal peristalsis by either a myogenic or neural mechanism.
本研究的目的是确定推注压力变化对食管蠕动的影响。在五只猫中,通过使用压力袖带压迫腹部将胃内压提高到20 - 45 mmHg来改变推注压力。在每只猫中,在食管蠕动期间,当食团位于食管远端时,胃内压的升高与食管食团压力的相应升高相关。通过同步视频荧光检查和食管测压记录向食管近端注射5 ml钡剂诱导的继发性蠕动。推注压力的分级增加导致无效、不完全蠕动序列的发生率增加,这些序列不能完全清除食管中的钡剂。当胃内压大于45 mmHg时,63%的蠕动序列不完全。胃内压升高引起的推注压力增加还导致:1)食管远端蠕动波减慢;2)食管远端压力波持续时间增加;(3)食管直径增加;4)食管下括约肌开放持续时间增加。逆行食团逃逸的发生率与蠕动波幅度和推注压力之间的差异呈负相关。大于20 mmHg的压力差可防止钡剂在食管各段逆行逃逸,而小于20 mmHg的差异通常与钡剂在食管远端逆行逃逸有关。我们得出结论,推注压力的增加会导致食管扩张增加,这通过肌源性或神经机制转化为食管蠕动的改变。