Effect of acute physical and psychological stress on gut autonomic innervation in irritable bowel syndrome

BACKGROUND & AIMS: Stress is an important causative factor in irritable bowel syndrome (IBS). It remains unknown whether stress-related changes in gut function are mediated by altered autonomic efferent gut-specific innervation. We studied the effect of acute physical and psychological stress on autonomic innervation and visceral sensitivity in healthy volunteers and patients with IBS.

METHODS: Twenty-four patients (20 women) with constipation-predominant IBS and 12 healthy volunteers (8 women) underwent either physical (cold water hand immersion) or psychological (dichotomous listening) stress on separate occasions. Assessments included stress perception (visual analogue scale), gut-specific autonomic innervation (rectal mucosal blood flow [RMBF] by laser Doppler flowmetry), and viscerosomatic sensitivity (anal and rectal electrosensitivity).

RESULTS: Patients with IBS had a heightened baseline perception of stress (P < .01). RMBF decreased during physical stress (29.6% +/- 2.8% and 28.7% +/- 3.9%) and psychological stress (24.4% +/- 2.1% and 23.5% +/- 4.3%) in patients with IBS and controls, respectively (mean +/- SEM). During physical stress, rectal perception (23.2% +/- 6% vs .6% +/- 3% [IBS vs control group, P < .05]) and rectal pain thresholds (27.0% +/- 4% vs 1.3% +/- 5%, P < .001) decreased in patients with IBS only. Psychological stress reduced thresholds for rectal perception (19.4% +/- 6% vs 8% +/- 6%, P < .01) and rectal pain (28.4% +/- 4% vs 3.4% +/- 3.8%, P < .001) in patients with IBS only. Acute stress elevated anal perception thresholds in patients with IBS but not controls (physical stress: 14.7% +/- 14% vs -9.3% +/- 11%, P < .05; psychological stress: 24.7% +/- 9% vs 11% +/- 11%, P < .05).

CONCLUSIONS: Acute stress alters gut-specific efferent autonomic innervation in both controls and patients with IBS, although normalization is delayed in IBS. By contrast, only patients with IBS show heightened visceral sensation, suggesting involvement of a different regulatory mechanism, either central or peripheral.