Transient lower esophageal relaxations

Compelling evidence exists that transient LES relaxations are the most frequent mechanism for reflux during periods of normal LES pressure (> 10 mmHg). Transient LES relaxations occur independently of swallowing, are not accompanied by peristalsis, are accompanied by crural diaphragmatic inhibition, and persist for longer periods than do swallow-induced LES relaxations (> 10 seconds) [29], [30]. The dominant stimulus for transient LES relaxation is distension of the proximal stomach, not surprising given that transient LES relaxation is the physiological mechanism for belching [31]. Transient LES relaxation can be experimentally elicited by either gaseous distension of the stomach or distension of the proximal stomach with a barostat bag. Gastric distension activates vagal afferent mechanoreceptors in the gastric cardia that project to the nucleus tractus solitarii in the brainstem and subsequently to the dorsal motor nuclei of the vagus and finally to the myenteric plexus.

With respect to the role tLESRs play in GERD, it appears that it is not the number but the quality of the refluxate associated with these events. Prolonged manometric recordings have not consistently demonstrated an increased frequency of transient LES relaxations in GERD patients compared to normal controls [32]. However, the frequency of acid reflux (as opposed to gas reflux) during transient LES relaxations has consistently been reported to be greater in GERD patients [32]. The cause for this difference in the frequency of acid reflux during tLESRs is unclear and hypotheses include differences in EGJ morphology and differences in the acid environment of the proximal stomach.

While tLESRs typically account for up to 90% of reflux events in normal subjects or in GERD patients without hiatus hernia, patients with hiatus hernia have a more heterogeneous mechanistic profile with reflux episodes frequently occurring in the context of low LES pressure, straining, and swallowing [33]. These observations support the hypothesis that the functional integrity of the EGJ is dependent on both the intrinsic LES and extrinsic sphincteric function of the diaphragmatic hiatus. In essence, gastroesophageal reflux requires a "two hit phenomenon" to the EGJ. Patients with a normal EGJ require inhibition of both the intrinsic LES and extrinsic crural diaphragm for reflux to occur: physiologically this occurs only in the setting of a tLESR. In contrast, GERD patients, especially those with a hiatal hernia may exhibit pre-existing compromise of the hiatal sphincter. In that setting reflux can occur with only relaxation of the intrinsic LES, as may occur during periods of LES hypotension or even de-glutitive relaxation.

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