Effects of acute normovolemic anemia on gastric mucosal blood flow in rats: Role of nitric oxide

Abstract

The present study investigates the effects of acute normovolemic anemia induced by isovolemic hemodilution on gastric mucosal blood flow (GMBF), measured by hydrogen gas clearance, and on the oxygen and hemoglobin content in the gastric mucosa, estimated by reflectance spectrophotometry. GMBF significantly increased after 3 and 6 mL of isovolemic hemodilution (from 50 ± 5 to 70 ± 7 and 77 ± 6 mL · min−1 · 100 g−1, respectively; P < 0.05) compared with basal values (50 ± 5 · mL−1 · min−1 · 100 g−1; P < 0.05). Oxygen content remained unchanged, whereas hemoglobin concentration decreased in parallel with the decrease in hematocrit. In a second set of experiments, the role of endogenous nitric oxide (NO) as a possible mediator of the gastric vascular changes induced by hemodilution was investigated by using the specific inhibitor of NO biosynthesis, NG-monomethyl-l-arginine (l-NMMA). The increase in GMBF induced by 3 mL of isovolemic hemodilution (Δ 23 ± 7 mL · min−1 · 100 g−1) was attenuated in a dose-related manner with l-NMMA, 6.25 mg/kg IV (Δ 15 ± 4 mL · min−1 · 100 g−1) or 50 mg/kg IV (Δ 5 ± 2 mL · min−1 · 100 g−1 g; P < 0.05). The concurrent administration of l-arginine (the precursor of NO biosynthesis) abolished the effects of l-NMMA on GMBF changes. The current findings show that acute normovolemic anemia causes an increase in GMBF that is dependent on the endogenous formation of NO.