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Adenosine modulates oesophageal sensorimotor function in humans
  1. J M Remes-Troche,
  2. P Chahal,
  3. R Mudipalli,
  4. S S C Rao
  1. Section of Neurogastroenterology, Division of Gastroenterology-Hepatology, Department of Internal Medicine, University of Iowa Carver College of Medicine & Clinical Research Center, Iowa City, Iowa, USA
  1. Dr S S C Rao, The University of Iowa Hospital & Clinics, 200 Hawkins Drive, 4612 JCP, Iowa City, IA 52242, USA; Satish-rao{at}


Background and aims: Adenosine mediates somatic and visceral pain, but its effects on gut visceral nociception are unknown. The aim of the present study was to test the hypothesis that adenosine alters oesophageal sensorimotor function.

Methods: In a double-blind, randomised, placebo-controlled study, 14 healthy volunteers (M/F = 4/10) received either intravenous adenosine 100 μg/kg/min or placebo infusion. Prior to and during infusion, all subjects underwent stepwise graded oesophageal balloon distensions using impedance planimetry. Sensory responses and biomechanical properties were assessed and compared.

Results: Adenosine significantly lowered thresholds for first perception (median (25th–75th), cm H2O; 10 (10–20) vs 30 (20–30), p = 0.007), discomfort (40 (30–40) vs 50 (50–60), p = 0.011) and pain (50 (40–60) vs 70 (60–70), p = 0.007) when compared with placebo. Also, the median threshold pressures required to induce first perception (p = 0.017), discomfort (p = 0.024) and pain (p = 0.026) were lower when compared with baseline. The cross-sectional area of the oesophagus increased (p = 0.032), and the circumferential wall tension/strain relationship shifted to the left (the wall became stiffer) (p = 0.043) after adenosine, when compared with baseline or placebo.

Conclusions: Adenosine can induce visceral hyperalgesia and decrease oesophageal distensibility in humans. These evoked sensorimotor changes are similar to those described in patients with functional oesophageal (non-cardiac) chest pain. Thus, adenosine modulates oesophageal sensorimotor function and may play a role in the pathogenesis of functional chest pain.

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  • Competing interests: None.

  • Funding: JMR-T was supported by the AGA Jon I Isenberg International Scholar Award and SSCR was supported by grant DK57100-0441 from the National Institutes of Health, Bethesda and in part by grant RR00059 from the General Clinical Research Centers Program, National Center for Research Resources. This work was also supported by a Clinical Research Grant from the American College of Gastroenterology.

  • Ethics approval: The study was approved by the human subjects Institutional Review Board.