Abstract
Purpose: Adenosine lowers sensory thresholds and decreases distensibility of the esophagus suggesting that it may play a role in the pathogenesis of esophageal hypersensitivity (Neurogastro Mot 2006; 18: A713). However, it is not known whether the adenosine induced alterations in esophageal sensorimotor function of healthy humans are akin to those observed in patients with functional (non-cardiac) chest pain (FCP). Our aim was to compare the sensory and biomechanical properties of esophagus in patients with FCP with those of healthy controls during adenosine infusion. Methods: In a randomized, double-blind, placebo-controlled study, 14 healthy subjects (M/F = 4/10), received either adenosine or placebo infusion, IV at 100 μg/kg/min. During infusion, subjects underwent stepwise graded balloon distensions of the esophagus (EBDT) using impedance planimetry. Sensory responses and biomechanical properties were assessed. One hour before infusion, impedance planimetry was performed to assess baseline sensori-motor properties. EBDT was also performed in 14 matched patients with FCP (Rome II). Data were analyzed for 7 controls who received adenosine with 14 FCP patients using ANOVA and paired t test. Results: (Table, mean ± SEM). When compared to controls at baseline, FCP patients had lower thresholds for sensory perception (P < 0.05), larger (P < 0.05) Cross Sectional Area (CSA) and decreased (P < 0.05) esophageal wall strain. Also, in controls, during adenosine infusion, sensory thresholds decreased significantly (P < 0.05). The CSA and reactivity of the esophagus increased, whereas wall strain decreased (P < 0.05), when compared to baseline. Sensorimotor properties were similar between controls (after adenosine infusion) and FCP (P > 0.05). Conclusion: In healthy controls, the adenosine-induced changes in esophageal sensorimotor function, notably hypersensitivity and decreased distensibility, were identical to those observed in native patients with FCP. Thus, adenosine may be a key mediator in esophageal hyperalgesia and sensorimotor dysfunction of patients with functional chest pain.Table
Published Version
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