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ACID-INDUCED OESOPHAGEAL CONTRACTIONS; ROLE OF MAST CELLS AND SUBSTANCE P
Acid reflux into the oesophagus causes both pain and longitudinal muscle contraction; however, the precise pathways involved are uncertain. This study used isolated segments of a opossum oesophagus perfused with acid to investigate the pharmacological pathways. Thirty μm capsaicin and 100 μm substance P were used to desensitise the TRPV1 and substance P receptors and determine their role. The authors showed (figure) that acid perfusion causes oesophageal shortening, which was largely prevented by capsaicin and substance P desensitisation as well as by MEN1037, a specific neurokinin 2 receptor antagonist. They similarly showed that isolated longitudinal smooth muscle strip contractions were inhibited by the same procedures, although not by tetrodotoxin. The authors suggest that protons diffusing through the epithelium activate mast cells which produce mediators activating an axonal reflex which involves substance P release and subsequent longitudinal muscle contraction. These acid-induced sustained oesophageal contractions correlate with chest pain and these studies suggest novel ways in which these patients might be treated.
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Effect of neurokinin 2 receptor antagonist (MEN10376), substance P and capsaicin desensitisation on acid-induced oesophageal shortening. Grey bars represent control, white bars drug or treatment effect.
THE SEQUENTIAL TREATMENT REGIMEN FOR HELICOBACTER PYLORI ERADICATION
H pylori eradication treatments are becoming less effective with at least 25% of patients failing standard 7–10 day triple regimens. New approaches to eradicating H pylori have been developed, including the so-called sequential therapy, based on a proton pump inhibitor (PPI), amoxicillin, …
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