Effect of straining on diaphragmatic crura with identification of the straining-crural reflex. The "reflex theory" in gastroesophageal competence

Abstract

Background. The role of the crural diaphragm during increased intra-abdominal pressure is not exactly known. We investigated the hypothesis that the crural diaphragm undergoes reflex phasic contraction on elevation of the intra-abdominal pressure with a resulting increase of the lower esophageal pressure and prevention of gastro-esophageal reflux. Methods. The esophageal pressure and crural diaphragm electromyographic responses to straining were recorded in 16 subjects (10 men, 6 women, age 36.6±11.2 SD years) during abdominal hernia repair. The electromyogram of crural diaphragm was recorded by needle electrode inserted into the crural diaphragm, and the lower esophageal pressure by a saline-perfused catheter. The study was repeated after crural anesthetization and after crural infiltration with saline. Results. The crural diaphragm exhibited resting electromyographic activity which showed a significant increase on sudden (coughing, p<0.001) or slow sustained (p<0.01) straining with a mean latency of 29.6±4.7 and 31.4±4.5 ms, respectively. Straining led to elevation of the lower esophageal pressure which was coupled with the increased electromyographic activity of the crural diaphragm. The crural response to straining did not occur during crural diaphragm anesthetization, while was not affected by saline infiltration. The lower esophageal pressure declined on crural diaphragm anesthetization. Conclusions. Straining effected an increase of the electromyographic activity of the crural diaphragm and of the lower esophageal pressure. This effect is suggested to be reflex in nature and to be mediated through the "straining-crural reflex". The crural diaphragm seems to play a role in the lower esophageal competence mechanism. Further studies are required to assess the clinical significance of the current results in gastro-esophageal reflux disease and hiatus hernia. © 2004 Shafik et al., licensee BioMed Central Ltd.