Citric acid strongly inhibits visceral pain response in mice
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Date
2008-04-17
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Abstract
Citric acid introduced into the stomach of mice at increasing concentrations of 0.1, 1 or 10 %
(4.8 µM-0.48 mM; 95 µmol/kg-9.5 mmol/kg, 0.5 ml) caused dose-dependent inhibition of
abdominal constrictions induced 1 h later by i. p. acetic acid injection by -51 % to -69.5 %.
When administered at 10 % (0.48 mM, 0.5 ml) 15 min before nociceptive challenge, citric
acid inhibited the nociceptive response by 96.8 %. Inhibition of the acetic acid-induced abdominal
constrictions was also observed when lower doses of citric acid were introduced into
the stomach (0.2 ml of 0.1-1 %; 38.1 µmol/kg-0.38 mmol/kg). The effect was evident as early
as 5 min after administration of citric acid into the stomach and with the maximal effect being
at 15-30 min after dosing. Lidocaine given orally 5 min prior to citric acid (1 %, 48 µM;
0.38 mmol/kg, 0.2 ml) prevented antinociception by citric acid, but lidocaine given 15 min
before oral introduction of citric acid enhanced the citric acid-induced inhibition of the nociceptive
response to acetic acid. The antinociceptive effect of orally administered citric acid
(1 %, 48 µM; 0.38 mmol/kg, 0.2 ml) was increased by pre-treatment with propranolol
(4 mg/kg, s. c.), yohimbine (4 mg/kg, s. c.), guanethidine (32 mg/kg, s. c.), but reduced after
treatment with atropine (3 mg/kg, s. c.), which itself increased the nociceptive behavior. Similar
inhibition of the acetic acid-induced nociceptive behavior was also observed when sodium
citrate (pH 7.21) or 0.1 N HCl (pH 3) or 1 % sucrose solution (0.2 ml) was intragastrically
given. It is suggested that citric acid might act to stimulate sensory afferents and that transmission
of nociceptive information centrally leads to the activation of descending antinociceptive
mechanism to a noxious stimulus.
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Keywords
citric acid, intraperitoneal acetic acid, mice, visceral nociceptive pain