Feeding ecology of indigenous and non-indigenous fish species within the family Sphyraenidae.

The feeding ecology of two common indigenous (Sphyraena viridensis and Sphyraena sphyraena) and one abundant non-indigenous sphyraenid species, Sphyraena chrysotaenia, of Indo-Pacific Ocean origin, was investigated in an area of the eastern Mediterranean Sea. The stomach contents of 738 individuals of varying size, collected during the period December 2008 to August 2009, were examined. The dietary analyses revealed that all three species were specialized piscivores with a diet consisting of >90% fish, both by number and mass. Concurrent sampling of the fish assemblage made it possible to calculate selectivity as well as diet breadth and overlap of these strict piscivores. Even though several prey species were found in the stomachs of the three predators examined, selectivity towards Atherina boyeri was highly significant. For all species examined, >70% of the diet by mass was made up by three indigenous species of commercial value: Spicara smaris, Boops boops and A. boyeri. Diet breadth and size of prey increased with increasing body size for all predators. With increased body size, the diet overlap between indigenous and non-indigenous species decreased. This could be attributed to increased diet breadth and the specific life-history characteristics of indigenous species developing into larger individuals. During winter, the condition factor of the non-indigenous species was significantly lower than that of the indigenous, indicating that winter conditions in the Mediterranean Sea may limit its further expansion north and westward. With this study, the gap in knowledge of the feeding preferences of the most abundant piscivorous species found in coastal areas of the study region is filled. Additionally, the results indicate that non-indigenous species familial affiliation to indigenous ones does not facilitate invasion success.

Diversity, structure and function of fish assemblages associated with Posidonia oceanica beds in an area of the eastern Mediterranean Sea and the role of non-indigenous species.

Temporal and spatial variation in density, biomass and body size of littoral fish species associated with nearshore Posidonia oceanica meadows was studied over an annual cycle in an area of the eastern Mediterranean Sea. A total of 109,350 littoral fishes were collected, belonging to 34 families and 88 species. Density of fishes peaked during the summer due to high numbers of juveniles. Season was a significant factor determining density, although number of species and biomass did not show any obvious seasonal pattern. Throughout the study, schooling planktivorous fish species such as the picarel Spicara smaris, the bogue Boops boops and the damselfish Chromis chromis were dominant, both in terms of density (80%) and biomass (70%). Temporal variation in density and body size of fishes was used to assess the seasonal and ontogenetic habitat use of each species, with their affinity to seagrass assessed by comparing their respective distribution on sand. Four functional guilds were created (juvenile migrants, seagrass residents, seasonal migrants and occasional visitors) to describe the habitat use of P. oceanica meadows by each species. Several species associated with P. oceanica meadows used this habitat mainly as juveniles during summer, although many others were present concurrently as adults and as juveniles. Among the species encountered, 11 were non-indigenous of Indo-Pacific origin, of which three used seagrasses mainly as juveniles and four as residents. The non-indigenous silverstripe blaasop Lagocephalus sceleratus ranked among the 10 most dominant species in terms of biomass (2%) and was classified as a seagrass resident.

Motility-induced but not vasoactive intestinal peptide-induced increase in luminal alkalinization in rat duodenum is dependent on luminal Cl(-).

AIM: to investigate whether the motility- and the vasoactive intestinal peptide (VIP)-induced increase in luminal alkalinization in the duodenum is dependent on luminal Cl(-). METHODS: experiments were performed in anaesthetized rats in vivo. The proximal duodenum was perfused luminally with an isotonic solution, containing zero or low Cl(-) and the effects on luminal alkalinization, motility, fluid flux and epithelial permeability were determined. Parecoxib, a COX-2 inhibitor, was used to induce duodenal contractions. RESULTS: control rats lacked duodenal wall contractions while parecoxib-treated ones exhibited contractions throughout the experiment. Most animals had a net fluid absorption during the perfusion with isotonic NaCl. Luminal alkalinization was about 100% higher in parecoxib-treated rats than in controls. Cl(-) -free solutions did not affect epithelial permeability or motility but decreased luminal alkalinization by ≥50% and decreased net fluid absorption in both control and parecoxib-treated animals. Reduction in luminal Cl(-) decreased alkalinization in a concentration-dependent manner. The parecoxib-induced increase in alkalinization was markedly reduced in the absence of luminal Cl(-) . VIP increased luminal alkalinization and induced fluid secretion. The lack of luminal Cl(-) did not affect the VIP-induced increase in alkalinization but reduced fluid secretion. CONCLUSIONS: the parecoxib-induced increase in luminal alkalinization is highly dependent on luminal Cl(-) and it is proposed that COX-2 inhibition, via induction of duodenal motility, enhances HCO(3) (-) efflux through stimulation of apical Cl(-) /HCO(3) (-) exchange in duodenal epithelial cells. Although the VIP-induced stimulation of fluid secretion is partly dependent on luminal Cl(-) , the VIP-induced increase in luminal alkalinization is not.

Comparative study of the effect of luminal hypotonicity on mucosal permeability in rat upper gastrointestinal tract.

AIM: To investigate whether the increase in mucosal permeability in the duodenum, induced by luminal hypotonicity, also occurs in the stomach and the jejunum and whether this increase in permeability can be explained by epithelial injury. METHODS: The stomach, duodenum or jejunum of the anaesthetized rat were perfused with a hypotonic solution and effects on mucosal permeability (blood-to-lumen clearance of radioactive probes); luminal alkalinization and net fluid flux were determined in the absence and presence of cyclooxygenase inhibition. RESULTS: The hypotonicity-induced (50 mM NaCl) increase in duodenal mucosal permeability was markedly larger in cyclooxygenase-2-inhibited animals than in controls and associated with a 20% decrease in luminal alkalinization and increased fluid absorption. Perfusion with 50 mM NaCl increased duodenal mucosal permeability to all probes investigated, i.e. (14)C-urea, (14)C-methyl-D-glucose, (51)Cr-EDTA and (14)C-inulin. The percentage increase in permeability was the greatest for inulin and the lowest for urea. Luminal hypotonicity caused superficial villous tip damage in some but not in all duodenal specimens but there was no difference in morphology between controls and cyclooxygenase-2-inhibited animals. Jejunum, but not the stomach, responded to luminal hypotonicity by increasing net fluid absorption, mucosal permeability (greater than sixfold) and the rate of luminal alkalinization (>100%). CONCLUSIONS: The stomach does not respond while the jejunum is more sensitive to hypotonicity-induced increase in mucosal permeability than the duodenum. The hypotonicity-induced increase in duodenal mucosal permeability most probably constitutes a physiological mechanism that entails widening of paracellular pathways, which facilitates the transport of osmolytes into the lumen.

Products of cyclooxygenase-2 depress duodenal function in rats subjected to abdominal surgery.

AIM: Abdominal surgery evokes powerful biological responses that affect gastrointestinal functions. Here we investigate the role of the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoforms in post-operative duodenal ileus. METHODS: Proximal duodenum of anesthetized rats was perfused in situ with isotonic or hypotonic (50 mM) NaCl. Mucosal bicarbonate secretion, motility, mucosal permeability and effluent osmolality were determined in the absence and presence of different COX inhibitors. RESULTS: The majority of control animals had no or few duodenal contractions and bicarbonate secretion averaged 10.9 +/- 1.4 micromol cm(-1) h(-1). These 'paralytic' controls responded to hypotonic NaCl with a small increase in mucosal permeability. In control animals exhibiting spontaneous duodenal contractions, the bicarbonate secretion was 50% higher and the hypotonicity-induced net increase in mucosal permeability sevenfold higher than in 'paralytic' controls. Treatment with the selective COX-2 inhibitors rofecoxib or parecoxib induced duodenal motility, increased bicarbonate secretion and potentiated the hypotonicity-induced increase in mucosal permeability. COX-2-inhibited animals had a twofold greater capacity to adjust luminal osmolality than 'paralytic' controls. The selective COX-1 inhibitor SC-560 only transiently stimulated motility and bicarbonate secretion and the hypotonicity-induced increase in mucosal permeability was smaller than in COX-2-inhibited animals. CONCLUSIONS: Abdominal surgery increases the synthesis of prostanoids, particularly via the COX-2 isoform. This compromises the ability of the duodenum to contract and to secrete HCO and to adjust luminal osmolality possibly via altered mucosal permeability. It is proposed that studies of gastrointestinal functions in animals subjected to abdominal surgery should include animals pre-treated with a COX-2 inhibitor.

Luminal hypotonicity increases duodenal mucosal permeability by a mechanism involving 5-hydroxytryptamine.

AIM: To investigate whether 5-hydroxytryptamine (5-HT) participates in the mediation of the hypotonicity-induced increase in duodenal mucosal permeability. METHODS: Proximal duodenum in anaesthetized rats was perfused in situ with a hypotonic NaCl solution and effects on duodenal motility, net fluid flux, mucosal permeability [blood-to-lumen clearance of (51)Cr-ethylenediaminetetraacetic acid (EDTA)] and the release of 5-HT into the luminal solution studied in the presence of the cyclooxygenase inhibitor indomethacin. RESULTS: Perfusion of the duodenum with 50 mm NaCl increased mucosal permeability eightfold, increased the luminal output of 5-HT twofold and induced net fluid absorption. This rise in permeability was enhanced 25% by 5-HT (3 x 10(-3) m), reduced by the 5-HT(3)-receptor antagonists granisetron (10(-4)-3 x 10(-4) m) or ondansetron (10(-5)-10(-4) m) or by the 5-HT(4) receptor antagonist SB 203186 (10(-4) m). The 5-HT(3/4) receptor antagonist tropisetron, at 10(-4) m, did not affect while 3 x 10(-4) and 3 x 10(-3) m augmented the hypotonicity-induced increase in mucosal permeability. Lidocaine (1.1 x 10(-3) m) similarly potentiated while tetrodotoxin (TTX) (5 x 10(-5) m) inhibited the hypotonicity-induced increase in mucosal permeability. Compared with animals treated with indomethacin alone ondansetron and granisetron augmented (by 30-40%) while tropisetron and lidocaine reduced (by 60-70%) the hypotonicity-induced net fluid absorption. Tetrodotoxin and all 5-HT receptor antagonists, except tropisetron, depressed duodenal motility. CONCLUSIONS: Luminal hypotonicity increases duodenal mucosal permeability by a neural mechanism involving 5-HT acting on 5-HT(3) and 5-HT(4) receptors. 5-HT also appears to participate in the regulation of the hypotonicity-induced fluid flux.