By use of an in vivo canine chambered stomach preparation in which the gastric mucosa was partitioned into two equal halves, the effect of topical 16,16-dimethyl PGE2 (DMPGE2) (1 microgram/ml of perfusate) and 8% and 40% ethanol on tissue levels of nonprotein sulfhydryl compounds was assessed. Both DMPGE2 and 8% ethanol significantly increased (P less than 0.005) mucosal levels of nonprotein sulfhydryls when compared with corresponding mucosa bathed with saline alone. In contrast, mucosa bathed with 40% ethanol showed significantly decreased levels. If mucosa was bathed with DMPGE2 or 8% ethanol prior to exposing the stomach to 40% ethanol, this depletion in sulfhydryl compounds was not observed. Since other experimental observations have shown that exogenously administered prostaglandins and mild irritants (such as low-dose alcohol) can prevent gastric mucosal damage by necrotizing agents (such as high-dose alcohol), our findings are consistent with the hypothesis that nonprotein sulfhydryls may play a role in mediating gastric mucosal protection.

Cardiac glycosides are known to inhibit cation transport and the activity of Na+-K+-dependent ATPase in most tissues (1). In oxygenated in vitro frog gastric mucosa Davenport (2) reported that ouabain inhibited active transport of H+ and Na+, and Cooperstein (3) observed inhibition of H+ and C1-transport with strophanthidin. In rat gastric mucosa Sernka and Hogben (4) found inhibition of active H+ and C1transport by ouabain.The purposes of our study were (a) to explore the effects of ouabain on active transpolt and the electrical properties of an in vivo canine stomach preparation and (b) to compare these findings with flux measurements in an in vitro canine stomach preparation. This comparison suggests that simpler measurements in the in vivo preparation permit prediction of findings in the in vitro.Materials and Methods. In vivo preparation. Six fasted mongrel dogs ( 13-22 kg) of either sex were anesthetized with intravenous chloralose and ethyl carbamate ( 1 ml/kg of a solution containing 9.25 g chloralose and 92.5 g ethyl carbamate in 150 ml normal saline). Our in vivo chambered stomach preparation has been described previously (5).The chamber divided the stomach flap into two sides. Each side was bathed with 10 ml of isotonic saline maintained at 37". The effluent from one side was collected and titrated (Radiometer autoburette) at 15 min interyals to determine the gastric acid output. The other side of the chamber was connected to calomel electrodes and Ag-AgC1 electrodes to determine transmural potential difference (PD) and current ( I ) necessary to reduce the PD to zero, respec-Recipient of Research Scientist Development Award 1 KO2 MH70463-0 1. tively . These measurements were determined with a Shanbour voltage-clamp system (6). The relative resistance (R) was then calculated as the ratio of PD to I . The pH of this side of the chamber was kept above 2.5 by constantly flushing the mucosa with normal saline at 3437".Histamine base (1.2-2.0 pg/kg min) was infused through a femoral vein for 90 min. Then, with continuous histamine infusion, ouabain (Lilly) was injected as a bolus dose (50 pg/kg) into the other femoral vein. Throughout both control and postouabain periods, measurements of PD, I , and acid output were obtained at intervals noted above. Only those animals which achieved an acid secretory rate above 60 pEq/ 15 min were used in the study.In vitro preparation.

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