The relative importance of HCO3- and blood flow in the protection of rat gastric mucosa during shock.

Recent research has shown adequate mucosal blood flow and blood bicarbonate availability to be crucial in the prevention of gastric ulceration, yet the relative importance of these two factors is unknown. We studied the incidence of ulceration in rats subjected to hypovolemic shock under varying conditions of blood flow and acid-base balance. At the start of the experiment 2 ml of 0.1 M HCl were instilled into the stomach. In the control series, severe systemic acidosis had developed after 2 h of shock (B.P. 40 mmHg) and 6 of 6 stomachs ulcerated. Mucosal blood flow, measured with radioactive microspheres, had drastically decreased. Prostacyclin dissolved in 0.01 M phosphate improved gastric blood flow but did not help to correct acidosis, and 6 of 8 stomachs ulcerated. A higher degree of protection was observed when the prostaglandin was dissolved in 0.16 M HCO3-. Intraarterial infusion of high concentrations of bicarbonate completely eliminated acidosis with ulceration occurring in 1 of 6 rats infused with 0.5 M and in 1 of 10 with 1 M bicarbonate. Blocking the carbonic anhydrase with acetazolamide (100 mg/kg) completely prevented the protective effect of a 1 M HCO3- infusion, and 6 out of 8 stomachs ulcerated. Substituting TRIS buffer for bicarbonate in the infusion also eliminated acidosis, but neither concentrations of 1 M or 5 M buffers prevented the stomachs from ulceration (6 out of 6 with 1 M buffer and 5 of 6 with 5 M buffer). We conclude that bicarbonate is the essential factor in prevention of ulceration in our shock model and that blood flow is also important as one component of a bicarbonate-dependent protection system involving carbonic anhydrase.