Selected Publication:
Evangelista, S; Renzi, D; Lippe, IT; Mantellini, P; Guzzi, P; Maggi, CA.
Intraluminal release of PGE2 due to gastric perfusion of urethane-anaesthetized rats with hydrochloric or taurocholic acid.
INT J TISSUE REACT. 1990; 12(4): 237-241.
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- Co-authors Med Uni Graz
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Lippe Irmgard Theresia
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- Abstract:
- We have measured the intragastric release of prostaglandin E2-like immunoreactivity (PGE2-li), pH changes and mucosal damage in response to gastric perfusion with hydrochloric or taurocholic acid at pH 1.5 in urethane-anaesthetized rats. Hydrochloric acid-perfusion caused a reversible decrease in pH values, no damage to the gastric mucosa and an intraluminal release of PGE2-li. Exposure to an ulcerogenic dose (25 mM) of taurocholic acid produced an intraluminal release of PGE2-li much higher than that of the non-ulcerogenic perfusion with hydrochloric acid. These findings indicate that intraluminal release of PGE2-li, thought to play a role as an endogenous antiulcer factor, can occur in response to a stimulus producing a significant damage of the gastric mucosa or to a mild irritant stimulus.
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Anesthesia -
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Animals -
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Dinoprostone - metabolism
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Hydrochloric Acid - administration and dosage
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Hydrogen-Ion Concentration - administration and dosage
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Immunoenzyme Techniques - administration and dosage
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Male - administration and dosage
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Perfusion - administration and dosage
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Rats - administration and dosage
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Rats, Inbred Strains - administration and dosage
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Stomach - metabolism
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Stomach Ulcer - chemically induced
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Taurocholic Acid - administration and dosage
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Time Factors - administration and dosage
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Urethane - administration and dosage