[The protective effect of systemic HCO3- administration on the gastric mucosa in 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 hypovolaemic 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 hours of shock (mean arterial blood pressure 40 mm Hg) and 6 out of 6 stomachs were 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 out of 8 stomachs were ulcerated. A higher degree of protection was observed when prostaglandin was dissolved in 0.16 M HCO-3. Intraarterial infusion of high concentrations of bicarbonate completely eliminated acidosis, with ulceration occurring in only 1 out of 6 rats infused with 0.5 M bicarbonate and in 1 out of 10 with 1 M bicarbonate. Blocking carbonic anhydrase with acetazolamide (100 mg/kg) completely prevented the protective effect of a 1 M HCO-3 infusion, and 6 out of 8 stomachs were ulcerated. Substituting TRIS buffer for bicarbonate in the infusion also eliminated acidosis, but neither concentrations of 1 M or 5 M buffer prevented the stomachs from ulceration (6 out of 6 with 1 M buffer and 5 out 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.