Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was carried out to measure gastro-oesophageal reflux in 6 asymptomatic and 9 heartburn subjects using a perfusion technique. Subjects swallowed a multi-lumen tube and the lower oesophageal sphincter pressure was measured. A phenol red solution was then infused through it into the stomach for 90 minutes whilst the oesophagus was aspirated continuously. The quantity of phenol red in oesophageal and gastric aspirates over 10-minutes periods was measured. In the heartburn subjects reflux was 1.27 +/- 0.37 ml/min and in the control subjects 0.23 +/- 0.07 ml/min, (p = 0.02). After 10 ml of an antacid combination, reflux in heartburn subjects was reduced to 0.59 +/- 0.18 ml/min and 0.68 +/- 0.16 ml/min in the second and third 30-minute period. Sphincter pressures increased from 8.9 to 11.8 mmHg. Control subjects showed little change in sphincter pressure or reflux after the antacid. Serum gastrin and secretin levels did not change in either group. This technique enables gastro-oesophageal flow rates to be easily measured. The results suggest that antacid administration tends to normalize lower oesophageal sphincter pressure and gastro-oesophageal reflux in patients with heartburn.
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PMID:Measurement of gastro-oesophageal reflux after antacid administration using a perfusion technique. 726 62

Gastro-oesophageal reflux and coronary artery disease frequently coexist. Stimulation of myocardial vagal receptors impairs lower oesophageal sphincter (LOS) function and may explain this link. This study examined the role of bradykinin, produced in increased quantities by the ischaemic myocardium, in activating this reflex. Thirteen dogs had patches soaked in bradykinin 100 micrograms/ml and saline applied sequentially to the left ventricular epicardium. Eleven of these animals were further divided into two subgroups: group 1 animals (six dogs) had the above sequence repeated after obliteration of sympathetic afferent fibres with phenol and those in group 2 (five animals) underwent sequential intravenous and intra-atrial injection of bradykinin 0.2 micrograms/kg. Epicardial bradykinin produced a fall in mean(s.e.m.) LOS tone from 13.3(1.3) to 6.0(0.5) sphinctometer units (P < 0.002), accompanied by a reduction in mean(s.e.m.) arterial pressure from 95(4) to 83(5) mmHg (P < 0.002). Destruction of sympathetic afferent fibres did not alter the LOS effect. Intra-atrial, but not intravenous, bradykinin reproduced the LOS effect; this suggests a cardiac origin. Myocardial release of bradykinin may play a role in producing transient LOS relaxation, predisposing to gastro-oesophageal reflux.
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PMID:Bradykinin, coronary artery disease and gastro-oesophageal reflux. 782 Apr 72