Gastric mucosal blood flow has a vital role in gastric mucosal protection. A high blood flow is considered a good protection against injury, as it dilutes, neutralizes, and removes hazardous substances that have penetrated the gastric mucosal barrier. A research group in Sweden has previously found that a water extract of H. pylori reduces the mucosal blood flow in rats by a mast cell- and platelet activating factor (PAF)-dependent pathway.
In this study they further investigated the mechanisms behind the reduction in blood flow in mice. This will be published on January 14, 2009 in the World Journal of Gastroenterology.
In their study, the stomachs of isoflurane-anesthetized mice were exteriorized, and the mucosal surface exposed. Blood flow was measured with the laser-Doppler technique, and systemic arterial blood pressure monitored. C57BL/6 mice were exposed to water extract produced from H. pylori strain 88-23. To investigate the role of a nerveor iNOS-mediated pathway, they used intraluminal lidocaine and iNOS-/- mice. Blood flow response to the endogenous nitric oxide synthase inhibitor asymmetric dimethyl arginine (ADMA) was also assessed.
They found that in wild-type mice, the water extract of H. pylori decreased mucosal blood flow by approximately 30%. This reduction was abolished in iNOS-deficient mice, and by pre-treatment with lidocaine. Luminally applied ADMA resulted in reduction in blood flow similar to that observed in wild-type mice exposed to the water extract of H. pylori.
The results indicated that H. pylori water extract reduces gastric mucosal blood flow acutely through an iNOS- and nerve-mediated pathway. This will be very importance to understand the development of gastric inflammation.
Materials provided by World Journal of Gastroenterology. Note: Content may be edited for style and length.
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