Effects of natural winter pasture and commercial pellet on the ultrastructure of small intestinal epithelium in reindeer.

Segments of small intestine (duodenum, jejunum and ileum) from slaughtered reindeer (Rangifer tarandus tarandus) grazing natural winter pastures (n=3) and reindeer fed commercially available pellets (RF-80) in winter (n=5) were collected and immediately fixed in McDowell's fixative. Transmission electron microscopy was employed to investigate the ultrastructural features of the epithelium and lamina propria along the small intestine and to relate these to the different diets. Major differences in ultrastructural features were observed between the small intestinal enterocytes of reindeer fed the two diets. Enterocytes in reindeer fed the natural diet displayed a normal appearance with a dense cytoplasm and distinct microvilli. In contrast, reindeer fed the commercial diet showed damaged enterocytes amongst the normal cells. Abnormal changes included disintegration and loss of microvilli, cytoplasmic swelling, loss of membrane integrity and increases in the width of intercellular spaces, especially in the jejunum.

Effects of seasonal changes in food quality and food intake on the transport of sodium and butyrate across ruminal epithelium of reindeer.

Transport of 22Na and 14C-butyrate across the ruminal epithelium of captive reindeer fed a concentrate diet in summer (n=5) and in winter (n=5) and from free-ranging reindeer taken from summer (n=3) and winter pasture (n=5) was measured in vitro in Ussing chambers. Significant amounts of both Na+ and butyrate were transported across the isolated epithelium without any external driving force. The ruminal transport of Na+ and butyrate were interacting, as evidenced by both the observed amiloride-induced reduction of net butyrate-transport and by the positive correlation between net transport of butyrate and Na+. Amiloride also reduced the net transport of Na+ without significantly affecting the short-circuit current, indicating the presence of an apical Na+/H+ exchanger in the ruminal epithelium of reindeer. The captive reindeer increased the dry matter intake of a constant quality concentrate from winter to summer, but this neither affected their ruminal transport capacity nor their ruminal surface enlargement factor (SEF). Free-ranging reindeer increased their ruminal transport capacity for Na+ and butyrate from summer to winter but simultaneously reduced their ruminal SEF. The present data indicate that this food-induced increase in transport capacity was attributed to changes in the nutrient composition of the diet.

Physiological effects of seawater intake in adult harp seals during phase I of fasting.

Previous studies have shown that harp seals may drink considerable amounts of seawater. The current study was undertaken to study the physiological responses to bolus administration of seawater. Adult harp seals (Phoca groenlandica) were fasted without access to water for 48 h and then given 1000 or 1500 ml of seawater by a stomach tube. Changes in urine and plasma parameters were thereafter monitored for another 12-20 h. Urine production and urine excretion rate of Na+ and Cl- increased soon after administration and reached a maximum 3-4 h later. Urine osmolality was kept rather stable and high ( approximately 1500 mOsm x kg(-1)) following seawater administration, due to a drop in urine concentration of urea that was proportional to the simultaneous increase in urine concentration of NaCl. Plasma osmolality remained at approximately 340 mOsm x kg(-1), while plasma concentration of urea decreased some 20-25% due to increased excretion of urea when seawater was ingested. Despite bolus administrations of seawater of up to approximately 2% of body mass, homeostasis was maintained and no ill effects observed. It is concluded that the concentrating abilities of the kidneys of harp seals are sufficient to prevent net loss of body water following seawater ingestion. Seawater ingestion may, moreover, increase urinary osmotic space and thus serve as a mechanism to excrete additional urea produced during phase I of fasting.