Stressful Life Events, Acid Hypersecretion, and Ulcer Disease

Peters, Michael; Richardson, Charles T.

doi:10.1016/s0016-5085(83)80174-7

Cited by 87 publications

(39 citation statements)

References 37 publications

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“…The results of the preliminary study show that gastric responses to reserpine are dose dependent in that low doses (0 1-1 mg/kg) stimulate acid secretion, but have no adverse effects on the integrity of the mucosa, whereas high doses (5 mg/kg) depress this secretion and injure the mucosa. These findings are consistent with the knowledge that certain stressful events stimulate gastric acid secretion (Peters & Richardson, 1983) whereas others injure the gastric mucosa (Goldman & Rosoff, 1968) and, therefore, support the use of reserpine as an agent for the production of stress pharmacologically.…”

Section: Discussionsupporting

confidence: 90%

Reserpine, vagal adrenergic activity and stress‐induced acute gastric mucosal injury in the rat.

Salim¹

1987

The Journal of Physiology

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SUMMARY1. Stress activates the hypothalamus causing central adrenergic discharge and stimulation of the autonomic sympathetic system. Reserpine produces the same effect and, therefore, its acute gastric mucosal injury is stress-induced. This injury was employed in the gastric diversion rat, a model for determining gastric acid secretion under basal conditions, to examine the relationship of the vagus nerve to the autonomic sympathetic system in the mechanism of stress-induced acute gastric mucosal injury.2. After 6 h of reserpine (5 mg/kg i.P.), all rats developed oval or round lesions confined to the glandular stomach and of no constant relationship to rugal crests (lesion score 29+ 2-7 mm2, mean +S.E., n = 10). Microscopically, these lesions were vascular in origin, developing as intramural foci of haemorrhage or necrosis and expanding to communicate with the lumen. Pre-treatment with potent antisecretory doses of the anticholinergic atropine (5 mg/kg i.P.) or the H2-receptor antagonist cimetidine (40 mg/kg i.P.) did not influence this reserpine action (28 + 3 mm2 and 27-5 + 2'3 mm2, respectively, mean+ s.E., n = 10). Protection against the reserpine lesions by the a-adrenoceptor blocking drugs phenoxybenzamine or phentolamine given in a dose of 10 mg/kg i.P. was significantly (P < 0 01) more than that afforded by the 5 mg/kg i.P. dose. However, the 15 mg/kg i.P. dose was completely protective against the lesions. Vagotomy had a similar protective effect. Interruption of autonomic sympathetic delivery to the stomach by coeliac ganglionectomy had no influence on the macroscopic or microscopic effects of reserpine on the stomach (30 5 + 3-4 mm2, mean +s.E, n = 10).3. The H+ output associated with 6 h of gastric diversion (61 + 4-5 ,tmol, mean +S.E.) was significantly (P < 0-001) depressed by reserpine alone (26 + 2 jtmol) or with atropine (19+1-8,imol) or cimetidine (21+2,tmol). Protection against the reserpine lesions by phenoxybenzamine or phentolamine was associated with dosedependent increase of H+ output, which with the 15 mg/kg dose was similar to that of control values (58 + 4-1 ,tmol and 60-3 + 2-8 ,mol vs. 61 + 4-5 /tmol). Vagotomy protection was associated with an H+ output significantly (P < 0-001) lower than that with reserpine alone (14 + 1-4 jumol). Coeliac ganglionectomy had no influence on the H+ output associated with reserpine treatment.4. The results of this study suggest that in the rat stress produces vagal delivery of a-adrenoceptor stimulation to the stomach, causing vasoconstriction which depresses H+ secretion and induces mucosal injury. The autonomic sympathetic system does not participate in this stress-induced action. Since the gastric diversion rat was used in this study, the results also show that duodenal contents are not required for the development of stress-induced gastric mucosal injury and suggest that H+ is not a critical factor in its mechanism.

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Section: Discussionsupporting

confidence: 90%

Reserpine, vagal adrenergic activity and stress‐induced acute gastric mucosal injury in the rat.

Salim¹

1987

The Journal of Physiology

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“…26 Stress associated with this pace of societal change may also exacerbate GERD or make one more aware of their symptoms. [27][28][29] Dietary factors such as processed prepackaged "frozen" foods and "fast" foods are a reflection of this pace of change and pace of lifestyle in industrialized nations. These processed foods tend to be higher in fats and refined carbohydrates, factors well-known to be associated with increased risk of gastroesophageal reflux.…”

Section: Discussionmentioning

confidence: 99%

Changing Impact of Gastroesophageal Reflux in Medical and Otolaryngology Practice

et al. 2005

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During the 1990s, there was a substantial increase in the use of ambulatory care services for GERD. Although much of this increase was among the primary care community, otolaryngologists appeared to have an increasingly prominent role in the management of this disease. There have also been dramatic changes in physician prescribing patterns for GERD, with the emergence of the predominant role of proton pump inhibitors. However, the use of physician counseling for lifestyle modification of factors known to affect GERD remains very low. The increasing impact of GERD on physician practice emphasizes the importance of both physician and patient education in the delivery of health care related to this disease.

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“…Maladaptive behavioral and lifestyle patterns, chemical dependencies, alcohol abuse, and sleep disorders may also develop [Sauter et al;1990;Cahill, 1990]. Stress has been associated with hyperacidity and peptic ulcer formation, as well as other pathological gastrointestinal conditions [Holtmann et al 1990;Peters and Richardson, 1983]. Exacerbation of respiratory disorders, most prominently, asthma, has long been associated with stress, a relationship recently confirmed by laboratory evaluation [Kotes et al, 1989].…”

Section: Introductionmentioning

confidence: 99%

Stress among package truck drivers

et al. 1997

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In 1992, a cross-sectional questionnaire study of package truck drivers in one company was conducted at four widely scattered sites throughout the US; 317 drivers participated, representing 82% of those eligible. The package truck drivers scored significantly above the US working population comparison norm on all summary and individual scales derived from the SCL 90-R, indicating a substantial increase in psychologic distress for this group. The Global Severity Index, the best single summary measure of psychological distress in the SCL 90-R, revealed a mean T score for the drivers of 64.20, 91st percentile of the normative population. The group perceived significantly more daily stressful events than the average working adult, and their sensitivity to these events was also increased. Role overload, a component of the Occupational Stress Inventory, was the most consistent factor associated with symptoms of psychological distress on multiple regression analysis. This study suggests that job stress is a psychological health hazard for these drivers.

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Stressful Life Events, Acid Hypersecretion, and Ulcer Disease

Cited by 87 publications

References 37 publications

Reserpine, vagal adrenergic activity and stress‐induced acute gastric mucosal injury in the rat.

Reserpine, vagal adrenergic activity and stress‐induced acute gastric mucosal injury in the rat.

Changing Impact of Gastroesophageal Reflux in Medical and Otolaryngology Practice

Stress among package truck drivers

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