The effects of temperature and salinity on the blood chemistry and survival of juvenile Atlantic tarpon Megalops atlanticus.

Atlantic tarpon Megalops atlanticus are highly migratory sportfish that support recreational fisheries throughout their range. In US waters, juveniles can be found in coastal and estuarine habitats along the Gulf of Mexico and Atlantic seaboard, with temperature limiting their northern latitudinal distribution. Juveniles may overwinter in these areas during the first several years of life. Low temperatures are known to cause mortality in adults, but the challenges of temperature are less understood for juveniles. Furthermore, salinity, which can change dramatically in these habitats, may have a synergistic effect with temperature. To examine the physiological effects of temperature and salinity on juvenile tarpon, wild fish were acclimated to a range of conditions that potentially occur in the northern range of their estuarine habitats. The haematology of juvenile tarpon was examined in two salinity (≤2 and ≥30 ppt) and temperature (15 and 25°C) treatments, followed by a low-temperature tolerance test. After 2 weeks in treatment conditions, blood samples were analysed for haematocrit, pH, red blood cell concentration, haemoglobin content and plasma osmolality. Increased plasma osmolality was observed in fish at low temperature (15°C compared to 25°C) and at high salinity (≥30 ppt compared to ≤2 ppt). Blood pH was increased at 15°C compared to 25°C, with the highest pH at 15°C and low salinity. Haemoglobin, haematocrit and red blood cell concentration were higher at 25°C than 15°C, with haemoglobin lowest at 15°C and low salinity. For the low-temperature tolerance test, all fish were acclimated to 15°C for 2 weeks, then transferred to separate tanks where temperature was gradually decreased at 0.9 ± 0.1°C/h until fish lost equilibrium. Fish at low salinity lost equilibrium more rapidly (1 ppt, 12.65 ± 0.46°C) than fish at high salinity (30 ppt, 11.26 ± 0.14°C). The results indicate juvenile tarpon are susceptible to low temperature, which is exacerbated by low salinity, findings useful in the assessment of juvenile tarpon overwintering habitat.

Exacerbated brain edema in a rat streptozotocin model of hyperglycemic ischemic stroke: Evidence for involvement of blood-brain barrier Na-K-Cl cotransport and Na/H exchange.

Cerebral edema is exacerbated in diabetic ischemic stroke through poorly understood mechanisms. We showed previously that blood-brain barrier (BBB) Na-K-Cl cotransport (NKCC) and Na/H exchange (NHE) are major contributors to edema formation in normoglycemic ischemic stroke. Here, we investigated whether hyperglycemia-exacerbated edema involves changes in BBB NKCC and NHE expression and/or activity and whether inhibition of NKCC or NHE effectively reduces edema and injury in a type I diabetic model of hyperglycemic stroke. Cerebral microvascular endothelial cell (CMEC) NKCC and NHE abundances and activities were determined by Western blot, radioisotopic flux and microspectrofluorometric methods. Cerebral edema and Na in rats subjected to middle cerebral artery occlusion (MCAO) were assessed by nuclear magnetic resonance methods. Hyperglycemia exposures of 1-7d significantly increased CMEC NKCC and NHE abundance and activity. Subsequent exposure to ischemic factors caused more robust increases in NKCC and NHE activities than in normoglycemic CMEC. MCAO-induced edema and brain Na uptake were greater in hyperglycemic rats. Intravenous bumetanide and HOE-642 significantly attenuated edema, brain Na uptake and ischemic injury. Our findings provide evidence that BBB NKCC and NHE contribute to increased edema in hyperglycemic stroke, suggesting that these Na transporters are promising therapeutic targets for reducing damage in diabetic stroke.