Effects of chronic normovolemic anemia on gastric microcirculation and ethanol-induced gastric damage in rats

Abstract

The effects of chronic normovolemic anemia on gastric microcirculation and gastric mucosal susceptibility to ethanol-induced gastric damage were investigated in anesthetized rats. Blood exchange by a plasma expander during four consecutive days rendered the animals anemic with a 34% decrease in the baseline hematocrit but without affecting blood volume. Chronic anemia induced a decrease in whole blood viscosity, an increase in gastric mucosal blood flow measured by hydrogen gas clearance, a decrease in gastric vascular resistance, and a decrease in gastric hemoglobin content without changes in the gastric oxygen content, the latter two parameters being measured by reflectance spectrophotometry. Gastric mucosal blood flow was lowered by intragastric administration of 100% ethanol in both anemic and control rats, but the final blood flow was significantly higher in anemic than in control animals. Macroscopic gastric damage induced by ethanol administration was significantly lower in anemic than in control rats. We conclude that chronic normovolemic anemia increases gastric mucosal blood flow and leads a protecting mechanism against gastric mucosal damage induced by absolute ethanol.

Background Factors Associated with Postoperative Complications in Patients with Advanced Hypopharyngeal Cancers Undergoing Total Pharyngolaryngoesophagectomy Followed by Free Jejunal Flap Reconstruction

“…Diluting blood without changing blood volume improved microcirculation in an animal study, as blood viscosity decreases upon dilution. 12 Hemodilution has also been applied in the surgery of head and neck tumors. 13 For the cases in the present study, this mechanism may act to decrease complications.…”

Gastric Mucosal Blood Flow Changes in Helicobacter pylori Infection and NSAID‐Induced Gastric Injury

“…The relevance of GMBF decrease in the pathogenesis of NSAID-induced gastric damage is supported by the fact that NO donors are able to prevent such gastric lesions by restoring blood flow parameters [29]. Other drug-independent situations associated with GMBF changes such as mucosal hyperemia induced by acute or chronic normovolemic anemia also increase the resistance of the gastric mucosa to NSAIDS and other noxious agents [3,30]. Our own results suggest that the hyperemic response present in the early phase of H. pylori infection offers some protection against NSAID-induced gastric damage.…”