The effects of endotoxemia and fluid expansion on gastric hemodynamics and mucosal permeability in the baboon

The effects of sublethal intravenous endotoxin on gastric hemodynamics and mucosal ionic permeability were studied in eight adult baboons. Each baboon had construction of an internally drained Heidenhain pouch 2 weeks prior to testing. Ionic fluxes were determined by instillation and recovery of an acid test solution (ATS) containing 80 mM HCI and 80 mM NaCl. Four hours of endotoxemia resulted in significant decreases in cardiac output and mucosal blood flow to about one-half of control values. There was a small but insignificant increase in hydrogen back diffusion from -58 ± 26 to -131 ± 59 μequiv/ 30 min/100 cm² and no significant change in sodium flux from + 183 ± 44 μequiv/30 min/100 cm² with shock. Endotoxic shock resulted in a significant decrease in the transmucosal electrical PD from 40 ± 3 to 29 ± 4 mV with a significant increase in potassium flux from 6 ± 2 to 11 ± 3 μequiv/ 30 min/100 cm², both indicating mucosal damage. All pouches developed acute superficial erosions. Fluid resuscitation corrected blood flow and cardiac output without significantly changing ionic fluxes or potential difference. In the baboon, endotoxemia and its attendent ischemia in the presence of acid may result in clinically significant stress ulcers without significant increases in gastric mucosal ionic permeability.