Effect of Chronic Fear on the Gastric Secretion of HCl in Dogs

Mahl, George F.

doi:10.1097/00006842-194901000-00005

Cited by 54 publications

(29 citation statements)

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“…Modified sham feeding seems to adequately reflect normal physiological vagal activation of gastric secretion (18), which was confirmed by the observation that complete vagotomy abolished the acid response to sham feeding (19,20). The pathological mechanisms of stress ulceration nave otten been attnbuted to gastric hypersecretion (21)(22)(23). Pharmacological studies of brain neurotransmitters suggest that central GABAergic mechanisms are involved in the stimulation of gastric acid secretion in several species (7)(8)(9)(10)(11) and also participate in the aggravation of stress-induced ulceration.…”

Section: Discussionmentioning

confidence: 79%

GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.

Yamasaki

Gotō

Hara³

et al. 1991

Jpn.J.Pharmacol

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ABSTRACT-The effect of GABA agonists on vagal efferent activity was studied in anesthetized rats. PCPGABA, a GABAB agonist (4 and 8 mg/kg, s.c.), markedly activated the neural efferent discharge of the vagus. Muscimol, a GABAA agonist (0.1 and 0.3 mg/kg, i.v.), also facilitated vagal activity. Both agonists caused significant gastric acid hyperacidity. Bicuculline (0.25 mg/kg, i.v.) or picrotoxin (0.5 mg/kg, i.v.) given 10 min prior to each agonist had no effect on the frequency of vagal nerve firing elicited by PCPGABA (4 mg/kg, s.c.) or muscimol (0.3 mg/kg, i.v.). Pretreatment with scopolamine (0.25 mg/kg, i.v.) abolished PCPGABA stimulated vagal activity and gastric acid secretion. Methscopolamine (0.25 mg/kg, i.v.) inhibited only the hyperacidity evoked by PCPGABA, but not vagal activation. These results suggest that PCPGABA and muscimol may cause gastric acid secretion through central cholinergic descending mechanisms that are resistant to GABAA and GABAB antagonists.

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Section: Discussionmentioning

confidence: 79%

GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.

Yamasaki

Gotō

Hara³

et al. 1991

Jpn.J.Pharmacol

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“…The direct experimental evidence of HC1 secretion during fear or anxiety that was available at the outset of this series of studies was regarded as contradictory (26). Some of the previous reports indicated a positive relationship, some a negative one, and one suggested that the direction of change in HC1 secretion varied with the individual.…”

Section: Mahlmentioning

confidence: 89%

“…In a previous experiment (26) the gastric acidity and heart rate of dogs were measured during control conditions and during a modified conditioning procedure designed to produce chronic fear behavior. Considering the group of dogs as a whole, the experimental procedure resulted in chronic fear behavior and a significant increase in both the gastric acidity and the non-resting heart rate.…”

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confidence: 99%

Relationship between Acute and Chronic Fear and the Gastric Acidity and Blood Sugar Levels in Macaca mulatta Monkeys

Mahl¹

1952

Psychosomatic Medicine

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J_ HIS paper reports an investigation that is primarily a systematic study of hydrochloric acid secretion during acute and chronic fear. It also attempted to study the relationship between changes in gastric acidity and in blood sugar levels. The need for such an experiment arises from a previous study of chronic fear and hydrochloric acid secretion in dogs, from considerations of the applicability of Cannon's emergency hypothesis to. chronic emotions and the psychosomatic disorders, and from considerations of the etiology of peptic ulcer.In a previous experiment (26) the gastric acidity and heart rate of dogs were measured during control conditions and during a modified conditioning procedure designed to produce chronic fear behavior. Considering the group of dogs as a whole, the experimental procedure resulted in chronic fear behavior and a significant increase in both the gastric acidity and the non-resting heart rate.Cannon s theory of the emergency function of emotions (10) states that during rage and fear physiological changes occur which in general are a result of discharge over the sympathetic-adrenal division of the autonomic nervous system and simultaneous inhibition of the parasympathetic division. The resulting pattern of autonomic changes is regarded as the normal autonomic effector pattern of fear or anxiety, rage, and anger in an acuteemergency situation.Although the emergency theory was originally based on studies of acute responses, this

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“…My concerns had evolved from the experimental production of increased gastric (HC1) acid secretion in dogs, monkeys, and humans via the instigation of chronic anxiety in the laboratory to a desire to study variations in HC1 secretion in humans during spontaneously occurring, "real life" fluctuations in anxiety (Mahl, 1949(Mahl, , 1950(Mahl, , 1952Mahl & Brody, 1954;Mahl & Karpe, 1953). The intensive psychotherapeutic interview promised to be a fruitful situation for such research.…”

Section: The Initial Contextmentioning

confidence: 99%

Language in Psychotherapy

Russell¹

1987

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Effect of Chronic Fear on the Gastric Secretion of HCl in Dogs

Cited by 54 publications

References 0 publications

GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.

GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.

Relationship between Acute and Chronic Fear and the Gastric Acidity and Blood Sugar Levels in Macaca mulatta Monkeys

Language in Psychotherapy

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