Rat gastric mucosal oxygen tension, ulcer index, plasma gastrin and glucagon following restraint stress. Influence of vagotomy, splanchnicotomy and exogenous secretin.

Restraint stress ulcers in rats were developed and procedures evaluated designed at preservation of intact gastric microcirculation (pO2). Neither prior truncal vagotomy, splanchnicotomy nor combined dissection of abdominal autonomic nerves were effective in preventing the stress mediated fall of mucosal pO2 and the rise in plasma glucagon. The ulcer index remained elevated and gastrin essentially was unchanged. Prophylactic injection of increasing doses (1, 2, 4, 8, 16 U/kg secretin maintained microcirculation at pO2-levels subnormal for unstressed animals (Vmax 15.53 mm Hg; Km. 0.99 U/kg), but simultaneously brought about a continuous rise in serum gastrin. Up to 8 U/kg plasma glucagon was higher than in saline control groups reaching a peak value with 2 U/kg when ucler index showed its nadir. Secretin therapy (4, 8 U/kg) markedly improves both mucosal pO2 and ulcer index. It is suggested that breakdown of gastric microcirculation may not be solely responsible for stress ulcer development.