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The driving force for creation of channels in gastric mucus, for acid and pepsin transport, ismost probably the hydrostatic pressure generated within the gastric gland lumen. The aim ofthis study was to investigate the origin and regulation of the glandular pressure. In addition,several parameters known to play an important role in mucosal protection were investigated inrelation to glandular pressure. The study was performed in vivo in exposed gastric mucosa ofInactin@-anesthetized rats. Glandular pressure, epithelial cell surface pH and mucus gelthickness were measured with microelectrodes, mucosal blood flow by laser Dopplerflowmetry, and mucosal permeability by clearance of 51Cr-EDTA from blood to lumen.Specimens of mucosa were also investigated immunohistochemically. Actin immunostaining revealed muscle strands arising from muscularis mucosa and branchingat the gastric pits. Vasoactive intestinal peptide (VIP)- containing nerve fibers were found inclose relation to these muscle strands. Administration of VIP decreased glandular pressure,probably by relaxing the muscle strands. The glandular pressure decreased along with the reduction in acid/volume secretion whensecretagogue infusion was terminated or when acid secretion was blocked by ranitidine.Omeprazole administration, in contrast, sustained or increased the pressure despite totalinhibition of acid secretion, probably by increasing resistance to outflow of the glands,resulting in intraglandular volume accumulation and dilatation of the glands. Prostaglandin E2 greatly increased glandular pressure in low doses that did not affect bloodflow, acid secretion or mucus thickness, while indomethacin decreased the pressure.Aggressive factors (ethanol and HCl) applied topically increased the pressure, probably byreleasing prostaglandins, since indomethacin pretreatment inhibited this response. Topical administration of acid (pH 1) increased permeability and blood flow in the nonacid-secreting mucosa and decreased epi

The functional status of organ systems involved into the processing of exogenous food is critical for the survival and growth of fish early life stages. The present study on laboratory-reared larval turbot, Scophthalmus maximus, provides an overview on the ontogeny of structure and functions involved in digestion, absorption and metabolism of nutrients. At start of exogenous feeding the intestine of larval turbot is anatomically differentiated, with enterocytes displaying an adult-type ultrastructure and being able to process lipids. At the microvillous border of the enterocytes, enzymes of contact digestion such as aminopeptidase are found. The ultrastructure of the exocrine pancreatic cells is fully differentiated from hatching onwards. Likewise, substantial activities of trypsin-type proteases are present. A stomach anlage exists in first-feeding larvae; however, the stomach becomes functional (appearance of gastric glands and pepsin secretion) only during metamorphosis. Liver parenchymal cells already display a functional ultrastructure during the endotrophic phase; with onset of exogenous feeding they develop pronounced diet-related changes of their energy stores. Larval respiration is not executed by the gills since respiratory surface of these structures develops only towards metamorphosis. The energy generation of larval muscle tissue depends on aerobic metabolism, whereas glycolytic activities start to increase at metamorphosis. In conclusion, two important patterns can be recognized in the development of turbot larvae: (1) The structure/function is differentiated at hatching or at the onset of exogenous feeding (afterwards it experiences mainly quantitative but not qualitative growth, i.e., intestine, exocrine pancreas, liver); or (2) the structure/function is absent in larvae and develops only during metamorphosis (i.e., gills, glycolytic muscle metabolism, stomach).