Gastroesophageal junction high-pressure zone (GEJHPZ) is comprised of various components which include intrinsic smooth muscle in the wall of the lower esophagus and upper stomach and extrinsic skeletal muscle (crural diaphragm) acting as a sphincter from outside the wall of the esophagus. In several of our prior studies (1,2) we have used simultaneous ultrasound and manometry with pharmacologic manipulation to study the anatomy and physiology of the various components of GEJHPZ in non-GERD subjects. High-frequency ultrasound was colocalized with manometric pressure and this catheter assembly was pulled distal to proximal from the stomach into the thoracic esophagus. This was performed during breath holding under full inspiration and full expiration. All pressures were referenced to intragastric pressure. The inferior margin of the right crus of the diaphragm (RCd) and the initiation of the pull-through (pull-through start position) were used as axial spatial references. Pull-throughs were performed before and after intravenous administration of atropine to attenuate the pressure from the muscarinic intrinsic sphincter components (smooth muscle components). The muscarinic contribution to the intrinsic sphincter was reconstructed by subtracting the postatropine pressure profiles from the preatropine pressure profiles referenced to the crural diaphragm on the ultrasound image. The muscarinic component of the intrinsic sphincter demonstrates two distinct peaks in both inspiration and expiration that are separated by roughly 1 cm during the displacement of the costal diaphragm from its inferior to its superior-most positions. The distal peak reflects the intrinsic pressure due to the gastric clasp and gastric sling muscles (GC/GS), whereas the proximal peak reflects the pressure due to the lower esophageal circular muscle sphincter (LEC) (Figure 1). By superimposing the three pressure curves (preatropine total pressures, postatropine atropine-resistant pressures, and the subtracted muscarinic pressure contribution), it was possible to separate and study each of the sphincteric components of the normal GEJHPZ individually and as an overlapping group for the first time in vivo and to determine how they move with respect to each other during respiration.
To determine the extent to which the muscarinic component of the intrinsic sphincter (subtracted curves) approximated the complete intrinsic sphincter, a second study was performed in which the crural diaphragm was pharmacologically paralyzed (the external sphincter, rather than the internal sphincters as in the previous study) to isolate directly the intrinsic sphincteric contribution to the GEJHPZ (1). Non-GERD subjects undergoing general anesthesia who were on a ventilator for nonesophageal surgery were evaluated in this study. Cisatracurium was given to the subjects to paralyze the crural diaphragm. The probe was withdrawn at a constant velocity, and ultrasound images and pressure tracings were recorded simultaneously during inspiratory pause on a ventilator. Ensemble averaging of pressure was performed and referenced to the inferior margin of the crural diaphragm, as in the previous atropine study. Comparisons were made between the intrinsic sphincter pressure profile from the cisatracurium study, and the muscarinic intrinsic sphincter pressure profile from the atropine study. Two pressure peaks in the same relative axial locations with respect to the crural diaphragm were found in both pressure profiles from both these studies (Figure 2), indicating that the muscarinic contribution to pressure with the double-peaked structure was a good approximation of the intrinsic component of the gastroesophageal sphincter.
Thus the intrinsic sphincter is composed of two components, a proximal component (LEC) that overlaps and moves with the crural sphincter, and a distal component at the junction between the gastric cardia and esophagus, formed by the GC/GS complex. These two components along with the crural diaphragm combine to make up the high-pressure zone of the distal esophagus and proximal stomach which acts as an antireflux barrier (1).
Using the same techniques, we (3), evaluated patients with GERD. The relative contributions of each of the components of the GEJHPZ in GERD patients were evaluated and compared with non-GERD subjects, to determine which abnormalities may predispose patients to reflux. In the GERD patients, the intrinsic sphincter pressure profiles displayed an absence of the distal pressure in both inspiration (Figure 3) and expiration, indicating an absence of muscarinic tone in the GC/GS complex. In addition, the proximal pressure in patients with GERD reflecting the LEC pressure was present in the same axial location relative to the crural diaphragm as in the non-GERD subjects, but was attenuated by approximately 50% in magnitude.