Abstract

Coffee irritates the gastric mucosa disrupting its barrier and increasing the risk of peptic ulcers. However, caffeine's contribution to these effects has not yet been elucidated. In this study we looked at the local effect of caffeine on the microcirculation and nitric oxide production in rats together with systemic marker of oxidative stress malondialdehyde as possible mechanisms whereby caffeine might participate in mucosal barrier impairment. Four groups of rats were anesthetized and administered as a bolus four different intraperitoneal doses of caffeine (0, 1, 10 and 50 mg kg(-1) b.wt.). The gastric submucosal microcirculation and nitric oxide production were then recorded for 2.5 hours by in situ microdialysis using the flow marker ethanol. At the completion of the experiments, plasma caffeine and malondialdehyde levels as well as morphological mucosal injury were determined. There were no major differences in the macro- or microscopic pictures of the mucosa among the groups. Local microcirculatory (ethanol out/in ratio) and nitric oxide monitoring failed to demonstrate statistically significant changes as did measurement of plasma malondialdehyde in response to caffeine injections. Caffeine per se seems unlikely to contribute to the gastric mucosal barrier injury associated with coffee consumption by alterations in nutritive blood flow, nitric oxide production or aggravation of systemic oxidative stress. This information is relevant for better understanding of the mechanisms involved in caffeine-mediated influences on gastric physiology in relation to the irritant effects of coffee.

Highlights

  • IntroductionCaffeine (contained in coffee, tea, caffeinated beverages, cocoa, chocolate etc.) is the most consumed stimulant drug of abuse worldwide

  • Caffeine is the most consumed stimulant drug of abuse worldwide

  • This is in agreement with the expected value (∼ 9 μmol l-1) calculated using extrapolation of data obtained from the probe calibration study, i.e. in case the concentration of total nitric oxide (NO) in the perfusate was close to zero (Fig. 3)

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Summary

Introduction

Caffeine (contained in coffee, tea, caffeinated beverages, cocoa, chocolate etc.) is the most consumed stimulant drug of abuse worldwide. Epidemiological data support its irritant role in stomach and esophagus in association with gastroesophageal reflux leading to enhanced risk of ulcers and cancer in the afflicted areas[1, 2] This irritant effect was confirmed in young asymptomatic individuals[3]. To elucidate the cause of the irritant nature of coffee to the stomach, focusing on the effects of isolated and purified (pharmacologically) active components of coffee would lead to more information. Of these components caffeine is the most studied. In this study we looked at the local effect of caffeine on the microcirculation and nitric oxide production in rats together with systemic marker of oxidative stress malondialdehyde as possible mechanisms whereby caffeine might participate in mucosal barrier impairment

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