Using omeprazole to link the components of the post-prandial alkaline tide in the spiny dogfish, Squalus acanthias.

After a meal, dogfish exhibit a metabolic alkalosis in the bloodstream and a marked excretion of basic equivalents across the gills to the external seawater. We used the H+, K+-ATPase pump inhibitor omeprazole to determine whether these post-prandial alkaline tide events were linked to secretion of H+ (accompanied by Cr) in the stomach. Sharks were fitted with indwelling stomach tubes for pretreatment with omeprazole (five doses of 5 mg omeprazole per kilogram over 48h) or comparable volumes of vehicle (saline containing 2% DMSO) and for sampling of gastric chyme. Fish were then fed an involuntary meal by means of the stomach tube consisting of minced flatfish muscle (2% of body mass) suspended in saline (4% of body mass total volume). Omeprazole pre-treatment delayed the post-prandial acidification of the gastric chyme, slowed the rise in CI- concentration of the chyme and altered the patterns of other ions, indicating inhibition of H+ and accompanying CI- secretion. Omeprazole also greatly attenuated the rise in arterial pH and bicarbonate concentrations and reduced the net excretion of basic equivalents to the water by 56% over 48h. Arterial blood CO2 pressure (PaCO2) and plasma ions were not substantially altered. These results indicate that elevated gastric H+ secretion (as HCI) in the digestive process is the major cause of the systemic metabolic alkalosis and the accompanying rise in base excretion across the gills that constitute the alkaline tide in the dogfish. [ABSTRACT FROM AUTHOR]