TY - JOUR
T1 - The differential mechanisms of mild irritants on adaptive cytoprotection
AU - CHO, C. H.
AU - KO, J. K.S.
AU - TANG, X. L.
PY - 1994
Y1 - 1994
N2 - The protective action of mild irritants has been established. However, the mechanisms as to how they antagonize the injurious action produced by the subsequent challenge with an ulcerogenic stimulus are still unclear. The present study examined the different protective mechanisms of an oral administration of the three mild irritants, 20% ethanol, 0.3 mol/L HCl or 5% NaCl against the gastric injurious actions of absolute ethanol in rats. In an attempt to clarify the pathways and mediators involved in the adaptive cytoprotection, [d‐Pro2, d‐Trp7,9]‐substance P (substance P antagonist), Nw‐nitro‐l‐arginine methyl ester (l‐Name), indomethacin, capsaicin, lidocaine, atropine or hexamethonium was given. The protective action of 20% ethanol but not the other two mild irritants, was antagonized by l‐Name, indomethacin and capsaicin, which are the inhibitors of nitric oxide (NO) and prostaglandins (PG) synthesis, and afferent sensory neuron blocker, respectively. Substance P antagonist, lidocaine or atropine given alone, prevented mucosal damage; however, only substance P antagonist enhanced the anti‐lesion action of 20% ethanol, while atropine and lidocaine increased the protective effect of NaCl and HCl. The three mild irritants increased the residual gastric secretion. Only 20% ethanol and 5% NaCl but not 0.3% HCl significantly increased the basal adherent mucus and also attenuated the mucus depletion by absolute ethanol. It is concluded that the cytoprotective action of either ethanol or NaCl seems to be mediated through the increase of residual gastric secretion and adherent mucus. In the ethanol‐treated group, these actions could act through the afferent sensory fibres, with NO and PG as the possible mediators. The antilesion action of HCl is partly contributed by the increase of residual gastric secretion through its dilution action. However, the protective factors and mediators involved in this action need further investigations.
AB - The protective action of mild irritants has been established. However, the mechanisms as to how they antagonize the injurious action produced by the subsequent challenge with an ulcerogenic stimulus are still unclear. The present study examined the different protective mechanisms of an oral administration of the three mild irritants, 20% ethanol, 0.3 mol/L HCl or 5% NaCl against the gastric injurious actions of absolute ethanol in rats. In an attempt to clarify the pathways and mediators involved in the adaptive cytoprotection, [d‐Pro2, d‐Trp7,9]‐substance P (substance P antagonist), Nw‐nitro‐l‐arginine methyl ester (l‐Name), indomethacin, capsaicin, lidocaine, atropine or hexamethonium was given. The protective action of 20% ethanol but not the other two mild irritants, was antagonized by l‐Name, indomethacin and capsaicin, which are the inhibitors of nitric oxide (NO) and prostaglandins (PG) synthesis, and afferent sensory neuron blocker, respectively. Substance P antagonist, lidocaine or atropine given alone, prevented mucosal damage; however, only substance P antagonist enhanced the anti‐lesion action of 20% ethanol, while atropine and lidocaine increased the protective effect of NaCl and HCl. The three mild irritants increased the residual gastric secretion. Only 20% ethanol and 5% NaCl but not 0.3% HCl significantly increased the basal adherent mucus and also attenuated the mucus depletion by absolute ethanol. It is concluded that the cytoprotective action of either ethanol or NaCl seems to be mediated through the increase of residual gastric secretion and adherent mucus. In the ethanol‐treated group, these actions could act through the afferent sensory fibres, with NO and PG as the possible mediators. The antilesion action of HCl is partly contributed by the increase of residual gastric secretion through its dilution action. However, the protective factors and mediators involved in this action need further investigations.
KW - ethanol
KW - gastric mucus
KW - gastric protection
KW - nitric oxide
KW - prostaglandins.
UR - http://www.scopus.com/inward/record.url?scp=0028726529&partnerID=8YFLogxK
U2 - 10.1111/j.1440-1746.1994.tb01297.x
DO - 10.1111/j.1440-1746.1994.tb01297.x
M3 - Journal article
C2 - 7533552
AN - SCOPUS:0028726529
SN - 0815-9319
VL - 9
SP - S24-S28
JO - Journal of Gastroenterology and Hepatology
JF - Journal of Gastroenterology and Hepatology
IS - S1
ER -