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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.
Finally, it seems that gastric distention is the only factor for which an involvement in the triggering of postprandial TLESRs has been established. However, two recent studies performed in healthy subjects tend to show that the mechanisms involved in induction of TLESRs by meal and artificial distention are different. The first study [12] shows that cholecystokinin (CCK) infusion does not modify the number of TLESRs induced by a gastric load of a dextrose solution while in the second study [13] CCK infusion increases the rate of TLESRs triggered by a balloon distention. However, the molecular forms of CCK used in the two studies were different (CCK-33 in the first study, CCK-8 in the second).
In conclusion, it is clear that gastric distention triggers TLESRs but it is not definitively demonstrated that gastric distention is the only factor involved in postprandial TLESRs.
References
1. Mittal RK, Holloway RH, Penagini R, Blackshaw LA, Dent J. Transient lower esophageal sphincter relaxation. Gastroenterology 1995;109:601-610.
2. Holloway RH, Penagini R, Ireland AC. Criteria for objective definition of transient lower esophageal sphincter relaxation. Am J Physiol 1995;2683:G128-G133.
3. Penagini R, Bartesaghi B, Conte D, Bianchi P. Rate of transient lower esophageal sphincter relaxations of healthy humans after eating a mixed nutrient meal: time course and comparison with fasting. Eur J Gastroenterol Hepatol 1992;4:35-38.
4. Holloway RH, Hongo M, Berger K, McCallum RW. Gastric distention: a mechanism for postprandial gastroesophageal reflux. Gastroenterology 1985;89:779-784.
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6. Martin CJ, Patrikios J, Dent J. Abolition of gas reflux and transient lower esophageal sphincter relaxation by vagal blockade in the dog. Gastroenterology 1986;91:890-896.
7. Franzi SJ, Martin CJ, Cox MR, Dent J. Response of canine lower esophageal sphincter to gastric distension. Am J Physiol 1990;259:G380-G385.
8. Andrews PLR, Grundy D, Scratcherd T. Vagal afferent discharge from mechanoreceptors in different regions of the ferret stomach. J Physiol London 1980;298:513-524.
9. Nebel OT, Castell DO. Lower esophageal sphincter pressure changes after food ingestion. Gastroenterology 1972;63:778-783.
10. Ireland AC, Lyrenas E, Tippett MD, Dent J, Holloway RH. Provocation of transient lower esophageal sphincter relaxations and gastroesophageal reflux by intraduodenal fat. Gastroenterology 1990;98:A361.
11. Mangano M, Picone A, Bianchi PA, Penagini R. High fat meals: do they really affect the competence of the oesophago-gastric junction? Neurogastroenterol Motil 1995;7:273.
12. Ledeboer M, Masclee AAM, Batstra MR, Jansen JBMJ, Lamers CBHW. Effect of cholecystokinin on lower oesophageal sphincter pressure and transient lower oesophageal sphincter relaxations in humans. Gut 1995;36:39-44.
13. Boulant J, Mathieu S, D'Amato M, Abergel A, Dapoigny M, Bommelaer G. Role of cholecystokinin and loxiglumide in the occurrence of transient lower esophageal sphincter relaxations in healthy subjects. Neurogastroenterol Motil 1996;8:163.
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