Extract of the full text
of this article appear below.
What is the effect of gastric distention on occurrence of transient lower esophageal sphincter relaxation?
J. Fioramonti (Toulouse)
It is now well recognized that transient lower esophageal sphincter relaxation (TLESR) is the most common mechanism underlying gastroesophageal reflux in normal subjects and in patients with reflux disease, while defective basal LES pressure is considered as a characteristic of patients with severe esophagitis [1]. TLESRs are now well defined in terms of duration, amplitude and relation with esophageal motility and are clearly distinguished from other spontaneous fluctuations in basal LES pressure [2]. It is also established that gastroesophageal reflux and TLESRs occur mainly after a meal. For example, in healthy volunteers, 0-2.5 TLESRs/30 min have been detected in the fasted state and 3.0-5.0/30 min in the first half an hour following a 700 kcal homogenized mixed meal [3]. However, the question arises to know whether the postprandial increase in TLESR occurrence results from meal volume, meal composition or both?
The answer to the question "does gastric distention induces TLESR?" is clearly yes. It has been shown in humans and animals that gastric distention modifies basal LES pressure but contradictory data have been accumulated. On the contrary, Holloway et al. have definitively shown in 1985 that, in healthy subjects and in patients with gastroesophageal reflux, gastric distention increases the rate of TLESRs [4]. They have shown that balloon distention of the stomach with volumes of 250 or 500 ml, that resulted in a feeling of fullness but not nausea or pain, induced a threefold to fourfold increase in the number of TLESRs. In dogs, gastroesophageal reflux occurs mainly in the postprandial period as in humans [5]. This animal species was then used as a model for investigation of the control of TLESR. Gastric insufflation of air induces TLESRs similar to those seen spontaneously after a meal [6]. Using this model, interruption of vagal conduction by cooling the nerves in the cervical region permitted to show that TLESRs involve a vago-vagal reflex [6]. The construction of two kinds of gastric pouches in dogs permitted also to show that the subcardiac region of the stomach is primarily responsible for triggering TLESRs induced by distention [7]. This finding is in agreement with the fact that this gastric area is the most sensitive to induce vagal afferent discharges by mechanical stimulation [8].
Another question may be: "Besides gastric distention are there other events able to trigger TLESRs?" Fatty foods are commonly considered detrimental in patients with gastroesophageal reflux. It has been shown that ingestion of oil decreases the basal lower esophageal pressure [9] but data on the effects of fat on TLESRs are contradictory. Intraduodenal infusion of fat has been found to increase the rate of TLESRs in patients with esophagitis [10] while in another study [11] performed in healthy subjects and in patients with reflux disease it has been shown that ingestion of high fat meal does not increase the number of TLESRs in comparison with a low fat equicaloric meal.
...
only available for members ()
|
