Esophageal Hypersensitivity Research Articles

Esophageal dysfunction in syndrome X

Syndrome X is defined as anginal chest pain accompanied by objective signs of ischemia on exercise testing or myocardial scintigraphy, but with angiographically “normal” coronary arteries. The etiology of this enticing syndrome is still not known. Besides myocardial ischemia, esophageal dysfunction and visceral hypersensitivity may play a role in the development of pain. The purpose of this study was to study esophageal function and visceral sensitivity in patients with syndrome X. Twenty consecutive patients with the diagnosis of syndrome X were investigated with esophageal manometry and a 24-hour pH recording. Visceral esophageal sensitivity was explored by balloon distention of the distal esophagus, as well as by instillation of acid. Twelve patients (67% of the 18 evaluated) had some abnormality on 24-hour pH monitoring; 2 had abnormal global acid exposure time (pH < 4) and 7 had symptoms coincidental with episodes of pH < 4. Seven patients (35%) had esophageal dysmotility including 5 with the “nutcracker” esophagus. Esophageal hypersensitivity to acid (n = 9) or distention (n = 13) was seen in 14 of the 20 patients. Eleven patients received acid suppressive therapy that resulted in amelioration of chest pain in 8 (73%). Thus, results suggest that esophageal hypersensitivity rather than gross functional abnormality is an important factor for the development of chest pain in patients with syndrome X, and that acid in the context of a hypersensitive esophagus is the main culprit. Acid suppression may ameliorate pain in a substantial proportion of patients.

Effect of opiate antagonists on stress-induced oesophageal hypersensitivity to distension

Effect of opiate antagonists on stress-induced oesophageal hypersensitivity to distension

Intra-oesophageal balloon distension and oesophageal sensation in humans

Intra-oesophageal balloon distension is a recognized stimulus for the assessment of oesophageal motor and sensory responses. It is increasingly being adopted by oesophageal laboratories, especially for the investigation of unexplained chest pain. The purpose of this paper is to review current knowledge concerning intra-oesophageal balloon distension. Perception of balloon distension is dependent upon demographic variables such as age, height and sex. Even when these are controlled for, patient groups are more sensitive to the stimulus than are healthy controls. This is true for patients with dysphagia and irritable bowel syndrome as well as those with unexplained chest pain. The role of intra-oesophageal balloon distension in determining oesophageal visceral hypersensitivity is outlined. In the investigation of unexplained chest pain, it may double the diagnostic yield of either acid perfusion or edrophonium provocation testing. Intra-oesophageal balloon distension has the potential to assess the response to therapy in patients with unexplained chest pain and has also been used in conjunction with cerebral evoked potential measurements to identify the afferent pathways involved. This technique provides another diagnostic tool that can readily be used in any oesophageal laboratory.

Reflux related symptoms in patients with normal oesophageal exposure to acid.

Several studies, using pH monitoring with event markers, have identified patients with normal oesophageal exposure to acid despite an apparent relation between symptoms and reflux episodes. In this series of 771 consecutive patients referred for 24 hour oesophageal pH monitoring, a probability calculation was used to evaluate the relation between symptoms and reflux episodes. Oesophageal exposure to acid was normal in 462 of 771 recordings (59.9%); despite this, 70.8% (327 of 462) of these patients used at least once the event marker. In 96 patients (12.5% of total patients) with normal oesophageal exposure to acid, there was a statistically significant association between symptoms and reflux episodes. The symptom cluster of such patients was similar to that usually seen in patients with gastro-oesophageal reflux disease, but symptoms like belching, bloating, and nausea were common thus overlapping with the symptom pattern of functional dyspepsia. In these patients both the duration and the minimum pH of reflux episodes (either symptom related or asymptomatic) were significantly shorter and higher, respectively, when compared with those of patients with gastro-oesophageal reflux disease. These results are consistent with the idea that oesophageal hypersensitivity to acid is the underlying pathophysiological feature of this syndrome.

Lower oesophageal sphincter hypersensitivity to opioid receptor stimulation in patients with idiopathic achalasia.

Impairment of non-cholinergic innervation of the lower oesophageal sphincter has been suggested in idiopathic achalasia. As opioid nerves are present in the lower oesophageal sphincter and opioid peptides affect lower oesophageal sphincter motility, the effect of an opioid agonist, morphine (100 micrograms/kg iv), and an opioid blocker, naloxone (80 micrograms/kg iv), on lower oesophageal sphincter motor function was assessed in 10 healthy subjects and in 10 patients with untreated idiopathic achalasia on separate days and in randomised order. In addition, in six of the patients, naloxone 0.8 mg iv was injected 60 minutes after morphine and recordings continued for a further five minutes. Lower oesophageal sphincter pressure was monitored by a sleeve device. In the healthy subjects morphine decreased (p < 0.01) resting lower oesophageal sphincter pressure by 4 (1) mm Hg (23 (8)%). In the achalasia patients the effect was more marked, lower oesophageal sphincter pressure being reduced (p < 0.01) by 11 (2) mm Hg (46 (8)%). Naloxone reversed lower oesophageal sphincter pressure to basal. Both absolute and percentage decreases after morphine were significantly greater (p < 0.05) in the achalasia patients than in the healthy subjects. Swallow induced lower oesophageal sphincter relaxation was significantly decreased (p < 0.05) by morphine in the healthy subjects but not in the achalasia patients. Naloxone had no effect on resting lower oesophageal sphincter pressure or swallow induced relaxation in either healthy subjects or achalasia patients. In conclusion achalasia patients are hypersensitive to the effect of morphine on resting lower oesophageal sphincter pressure. This finding is unlikely to be the result of a denervation process involving opioid nerves.

Supersensitivity of the chronically denervated feline heart.

Supersensitivity of the chronically denervated feline heart.