We read the recent article by Houghton et al (Gut 2007, Apr 19 [Epub ahead of print]), reporting that pregabalin, a new generation of α₂δ ligand, increased sensory thresholds to normal levels in 26 patients with irritable bowel syndrome (IBS) and baseline rectal hypersensitivity, in a randomised double blind, placebo controlled, parallel group study. The authors concluded that α₂δ ligands are worthy of further physiological and clinical investigations for diseases affecting gut sensory function. Experimental studies to date indicate that pregabalin prevents colorectal allodynia and hyperalgesia in rats exposed to intracolonic trinitrobenzene-sulphonic acid¹ or septic shock.² Visceral hyperalgesia and symptoms in IBS are, however, characterised by the absence of overt colonic damage or mucosal abnormality. In the study we describe here, pregabalin given orally in a rat non-inflammatory model of repeated tonic colorectal-distension-induced hypersensitivity³ prevented visceral hyperalgesia and blunted lumbosacral spinal neurone activation.

Adult male Sprague–Dawley rats with or without electrodes implanted in the abdominal muscles were given orally (po) either vehicle (water, 1 ml/rat) or pregabalin (10 or 30 mg/kg; Parke Davis, Fresnes, France) and placed individually in Bollman cages. After a 60 minute stabilisation period, basal abdominal contractions were monitored for 10 minutes, then isobaric colorectal distension …