Fig. 6. RIC preserves intestinal microcirculation via endogenous vasodilators nitric oxide and hydrogen sulfide.

Administration of NO-synthase inhibitor and H₂S-synthesizing enzyme inhibitors abolished a Stage 1 RIC and b Stage 2 RIC-mediated preservation of intestinal wall flow velocity (mm/s) measured with Doppler ultrasound. c Treatment with NaHS, exogenous donor of H₂S, improved intestinal wall flow velocity (mm/s), but not in the presence of H₂S-synthesizing enzyme inhibitors. Administration of NO-synthase inhibitor and H₂S-synthesizing enzyme inhibitors abolished the d, g Stage 1 RIC- and e, h Stage 2 RIC-mediated preservation of submucosal arteriole velocity (µm/s) and arteriole flow volume [(μm)³/s] respectively, measured using TPLSM in real time. f, i Treatment with NaHS improved submucosal arteriole velocity (µm/s) and arteriole flow volume [(μm)³/s] respectively, but not following administration of H₂S-synthesizing enzyme inhibitors. Data were compared using two-sided one-way ANOVA with post hoc Turkey test (n = 8 per group; minimum of 2 readings were obtained per group; **p < 0.01; ***p < 0.001). Data are presented as mean ± SEM. Source data are provided as a Source Data file.