THE EFFECT OF ACUTE EMOTIONAL-STRESS ON GASTRIC-ACID SECRETION IN NORMAL SUBJECTS AND DUODENAL-ULCER PATIENTS

Citation
Wh. Bresnick et al., THE EFFECT OF ACUTE EMOTIONAL-STRESS ON GASTRIC-ACID SECRETION IN NORMAL SUBJECTS AND DUODENAL-ULCER PATIENTS, Journal of clinical gastroenterology, 17(2), 1993, pp. 117-122
Citations number
23
Categorie Soggetti
Gastroenterology & Hepatology
ISSN journal
01920790
Volume
17
Issue
2
Year of publication
1993
Pages
117 - 122
Database
ISI
SICI code
0192-0790(1993)17:2<117:TEOAEO>2.0.ZU;2-T
Abstract
Emotional stress (ES) has been proposed as a possible factor in the pa thogenesis of duodenal ulcer (DU) disease. Modem, well-controlled stud ies on the effect of ES on gastric acid secretion (GAS) in both normal healthy subjects and patients with inactive DU are lacking. Ten norma l (N) men and 10 men with inactive DU were observed on 2 separate days . In random order, subjects either underwent dichotomous listening (DL ) to induce stress or a control (non-DL) test. In addition to measurin g GAS in 15-min periods, heart rate and blood pressure were measured e very 7.5 min, and visual analog scale measures of emotion (relaxation, anxiety, anger, tension, and depression) were monitored. Subjects und erwent 2 separate study days, 1 h of a basal period followed by 1 h of a DL session or 1 h of a basal period followed by 1 h of a non-DL con trol session; the order of the days was randomized. In both N and DU e motional stress by DL induced these parameters significantly: increase d heart rate; raised systolic and diastolic blood pressures (p < 0.01) ; increased anxiety, anger, and tension (p < 0.03); and decreased rela xation (p < 0.01). The non-DL control test did not alter cardiovascula r or emotion measures in either group. While ES did not alter GAS in N subjects, ES increased GAS when compared to the basal state (p < 0.02 ) and when compared to the control test (p = 0.07). We conclude that i n N subjects, DL induces mental and cardiovascular evidence of acute s tress but fails to alter GAS, and in patients with inactive DU, ES res ulted in similar mental and cardiovascular changes as observed in norm al subjects, yet was accompanied by an increase in GAS. These prelimin ary findings suggest that acute ES stimulates GAS in patients with DU disease.