Gastric mucosal blood flow changes in Helicobacter pylori infection and NSAID-induced gastric injury.

Abstract

The impact of H. pylori infection on gastric mucosal blood flow and NSAID-induced gastric damage is unclear. To study the effects of H. pylori infection on gastric mucosal blood flow, both at basal conditions and after NSAID exposure, and its relation with mucosal damage and nitric oxide production. Gastric mucosal blood flow, nitric oxide production and gastric damage were assessed in time after H. pylori SS1 or E. coli inoculation in mice. Experiments were conducted in basal conditions or after oral exposure to indomethacin (20 mg/kg). H. pylori infected mice exhibited a significant increase in gastric blood flow and gastric nitric oxide production 1 week after infection, but those parameters returned to basal levels by 4 weeks. NSAID challenge elicited a similar reduction in gastric blood flow [25-35%] in H. pylori-infected and control animals. However, only 1 week H. pylori-infected mice, which exhibited a significant baseline hyperemia, were able to maintain gastric blood flow values within the normal range after NSAID exposure. NSAID-induced gastric damage was increased in H. pylori-infected mice by 4 weeks, but not 1 week after infection. Underlying H. pylori infection aggravates acute NSAID-induced gastric damage. However, at early phases, gastric hyperemia associated with increased nitric oxide production may exert some protective role.