Introduction The region of unbuffered acidity on top of the gastric contents after a meal, known as the post-prandial acid pocket,¹is a chief aetiological factor responsible for the frequently experienced post-prandial reflux.

We previously developed an in vitromodel of the post-prandial acid pocket adhering to the physiological characteristics described in the clinical literature.²Here we further improve this in vitromodel to simulate the occurrence of reflux events and also evaluate some anti-reflux products.

Method A standard refluxogenic meal (McDonalds double sausage and egg McMuffin + black coffee) was blended with 40 ml 0.01 M HCl and transferred to the model stomach within a sealed water chamber. An acid pocket layer of 0.1 M HCl was applied to meet the established clinically measured parameters (70 ml and 2.5 cm depth). A reflux event was simulated by applying air pressure into the water chamber rapidly and the refluxate was captured in a syringe through the modelled lower oesophageal sphincter. The model was validated with two alginate-based anti-reflux products [UK manufactured Gaviscon Double Action (GDA) and USA manufactured Gaviscon Extra Strength (GES)].

Results Application of 50 ml of air to the in vitropost-prandial acid pocket model resulted in refluxate volume of 10 ml (SD 1.7 ml) which is a representative refluxate volume.³

GDA suppressed reflux in the model in a dose dependent manner with 20 ml maximum GDA dose completely supressing 5 sequential reflux events. 10 ml GDA dose let through 2.7 ml of the reflux (mean of 5 events) and 2.5ml GDA dose let through 5.9 ml of the reflux (mean of 5 events). 20 ml maximum dose of GES did not supress reflux and 7.0 ml of the reflux was let through at maximum dose (mean of 5 events).

Conclusion This in vitromodel is representative of a fed stomach via introduction of a classic refluxogenic meal. The post-prandial acid pocket that is modelled represents that described in clinical studies and the model takes into account the pressure changes during a reflux event.

Alginate raft forming anti-reflux products GDA and GES were chosen to validate the model and GDA was able to suppress reflux events in a dose dependent manner with maximum dose (20 ml) totally supressing all reflux events. In contrast GES that does not form a coherent buoyant raft⁴was a poor reflux suppressant.

This in vitromodel of reflux of the post-prandial acid pocket has potential to screen and evaluate test products without the need of clinical studies.

Disclosure of interest None Declared.

References

1. Fletcher, et al. Gastroenterology 2001;121:775–783

2. Fisher, et al. UEG Journal2014;2(Suppl 1):A578

3. Sifrim Gut 2005;54:175–178

4. Hampson, et al. Int J Pharm. 2005;294:137–147