The detection and quantification, in vivo and in real time, of hydrogen sulfide in ethanol-induced lesions in rat stomachs using an ion sensitive electrode.

INTRODUCTION: The development of electrochemical sensors for the detection of small molecules has already had a significant effect on the study of biology because of their selectivity and ability to measure low concentrations of small molecules that regulate various functions in living organisms. Hydrogen sulfide (H2S) is a gasotransmitter produced at low levels in several tissues including the stomach. Here, we propose a new method for detecting low concentrations of this transmitter in the rat stomach, in-vivo and in real time, with applications in pharmacology and physiology.
METHODS: Wistar rats fasted for 12h. Then, the control group was given an intragastrical dose of saline. l-Cysteine (50mg/kg) or dl-propargylglycine (50mg/kg) were administered to the test groups to modify the H2S levels. Ranitidine (50mg/kg), omeprazole (40mg/kg) or carbenoxolone (30mg/kg) were used as reference anti-ulcer drugs. Thirty minutes later, the electrode was inserted in the middle of the stomach cavity of the anesthetized animals. The basal levels of H2S were recorded every 5min for 30min. Next, gastric lesions were induced with pure ethanol, and the recording continued for 30 additional minutes.
RESULTS: The exogenous administration of an H2S precursor (l-cysteine) increased the level of this gasotransmitter whereas dl-propargylglycine, a selective inhibitor of the enzyme cystathionine γ lyase, reduced the total concentration of H2S. The administration of carbenoxolone, a gastroprotective, increased the total amount of H2S. However, the administration of the anti-secretors omeprazole and ranitidine did not modify the total concentration of H2S. DISCUSSION: This work provides the basis for a real-time analysis of the changes in-vivo of the gasotransmitter H2S in the normal and injured stomach and the exploration of the effect of drugs on the regulation of H2S.