Acute stress alters intestinal function of rainbow trout, Oncorhynchus mykiss (Walbaum)

Groups of rainbow trout (Oncorhynchus mykiss Walbaum) in feeding (guts filled with digesta) or food-deprived (3 days of diet deprivation) states were subjected to 15 min of acute stress. Blood samples and intestinal tissue were collected and prepared for physiological, chemical and ultrastructural analysis immediately before stress, and at 4 and 48 h post-stress. Haematocrit, plasma cortisol and lactate levels increased following stress, and the response appeared to be more pronounced in food-deprived than in fed fish. Plasma glucose appeared to increase more in fed fish. Stress did not seem to cause massive tissue damage as measured by cellular leakage of transaminase enzymes into the blood. Furthermore, the plasma oxidative stress marker malondialdehyde did not increase markedly following stress. The content of malondialdehyde did not change following stress neither in midgut nor hindgut sections, and nor did membrane lipid class and fatty acid compositions. Ultrastructural studies showed that stress caused significant widening of the tight junctions between enterocytes in the midgut, with little effect seen in the hindgut. Fed fish appeared to experience more damage than food-deprived fish as judged by the ultrastructural analysis. But these changes were to a large extent transient and cellular organization in the midgut had returned to normal values within 2 days. Intestinal paracellular permeability of the midgut increased 4 h post-stress and was further increased 48 h post-stress of food-deprived fish, whereas no effect was seen in fed trout. In hindgut of food-deprived fish, the permeability appeared to increase sometime after 4 h and was still elevated 48 h after stress. No change in permeability occurred in fed fish. The adherent microbial population level and composition in hindgut was significantly reduced following stress, while the level increased in faeces. This suggests that substantial amounts of mucus are peeled off following stress. It is concluded that, under the present experimental conditions, acute stress causes cellular alteration in rainbow trout gastrointestinal tract. Ultrastructural damages are mainly observed in midgut, but most changes appear to be transient returning to normal levels within 48 h. Changes in adherent intestine microbial population level and compositions together with increased intestinal paracellular permeability following acute stress suggest a possible increased susceptibility to bacterial infections after stress and that active feeding may have a protective role.