A method of simulation of spontaneous rupture of the esophagus and pathogenetic aspects of gastro- esophageal intraorgan hypertension syndrome: experimental study

We created and tested an experimental model of spontaneous rupture of the esophagus (SRE). The 1st group consisted of live animals (n=5), the 2nd group consisted of dead animals (n=5). In all experiments rupture of the esophageal wall was performed, which with this method of modeling occurred in the lower third of the esophagus in mediamagnatom segment on the left side. The length of the gap ranged from 2.5 to 4.0 cm, the pressure difference of the gap between dead and live animals amounted to 0.2 bar – it means direct influence of the tone of the surrounding tissues and structures on spontaneous rupture of the esophagus. The level of intraluminal pressure wall rupture of the esophagus in live animals is much higher than physiological intraluminal pressure that occurs during vomiting (0.15 to 0.20 bar) and in vivo is not observed. Within experiment we created models of the intraorgan hypertension of the esophagus and stomach, defined intraluminal pressure wall rupture of the esophagus (1.3 bar) and stomach (0.5 bar), and the ratio of the received data with the level of hypertension in the lumen of the esophagus and stomach during vomiting. It is shown that intraluminal pressure that occurs while vomittting, can result in Mallory–Weiss syndrome, however, it is impossible to break the wall of the esophagus at this pressure. SRE is most likely a variant of mechanical damage to the esophagus caused by discoordination of muscle contractions that occur during vomiting.

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