Gastric hyperacidity and mucosal damage caused by hypothermia correlate with increase in GABA concentrations of the rat brain

Eur J Pharmacol. 1991 Feb 26;194(1):77-81. doi: 10.1016/0014-2999(91)90126-b.

Abstract

The involvement of brain GABA mechanisms in acid secretion and maintenance of gastric mucosal integrity was studied in the anesthetized rat. Cold exposure lowered the rectal temperature and stimulated acid output in the anesthetized rat. The acid response to cold exposure was completely suppressed by surgical vagotomy. The substantial increase in brain GABA content evoked by pretreatment with aminooxyacetic acid (10 and 20 mg/kg s.c. x 3) significantly potentiated the gastric acid response to the cold exposure stress; suppression of the GABA content induced by semicarbazide (100 mg/kg s.c.) reduced the acid response to cold. Significant correlations were found between the brain GABA contents and the acid secretory activity and also between the GABA contents and the ulcer index of gastric lesions induced by the cold stress. These results indicate that hypothermia evoked by cold exposure stimulates gastric acid secretion and induces gastric lesions through central GABA mechanisms in the rat.

MeSH terms

  • Aminooxyacetic Acid / pharmacology
  • Anesthesia
  • Animals
  • Brain Chemistry* / drug effects
  • Cold Temperature
  • Gastric Acid / metabolism
  • Gastric Acid / physiology*
  • Hypothermia / complications*
  • Hypothermia / physiopathology
  • Male
  • Rats
  • Rats, Inbred Strains
  • Semicarbazides / pharmacology
  • Stomach Ulcer / etiology*
  • Stress, Psychological / physiopathology
  • Vagotomy
  • gamma-Aminobutyric Acid / metabolism*

Substances

  • Semicarbazides
  • Aminooxyacetic Acid
  • gamma-Aminobutyric Acid