TY - JOUR
T1 - Physiological impact of salinity increase at organism and red blood cell levels in the European flounder (Platichthys flesus)
AU - Jensen, F. B.
AU - Lecklin, T.
AU - Busk, M.
AU - Bury, N. R.
AU - Wilson, R. W.
AU - Wood, C. M.
AU - Grosell, M.
N1 - Funding Information:
The study was supported by the Danish Natural Science Research Council grants 9300995 and 9901765 (FBJ) and NSERC Canada (CMW and MG). CMW is supported by the Canada Research Chair Program. RWW and NRB were supported by a Royal Society Travel Grant. MG was supported by a Journal of Experimental Biology Travelling Fellowship. We thank Mrs. Annie Bach for skilled technical assistance. [SS]
PY - 2002/8/5
Y1 - 2002/8/5
N2 - Blood respiratory, acid-base, and ionic changes in response to hyperosmotic shock were studied in vivo and in vitro in the European flounder. One primary aim was to evaluate regulatory changes in red blood cell (RBC) volume and its interrelationship with blood O2 transporting properties. An acute increase in the ambient salinity from 10 to 30 ppt caused small but significant increases in extracellular osmolality (<20 mosM kg-1), [Na+], and [Cl-], which were corrected within 48 h. RBC volume was not significantly changed 3 h after the in vivo exposure to elevated salinity. A small metabolic acidosis was fully developed within 3 h, and this acidosis seemed responsible for a modest decrease in blood O2 affinity (i.e., increased P50-O2 tension at 50% O2 saturation). RBC organic phosphates were unchanged. In vitro elevation of whole blood extracellular osmolality by 60 mosM kg-1 caused immediate RBC shrinkage. The subsequent regulatory volume increase (RVI) showed a graded dependency on blood O2 saturation (SO2). At SO2 values of 0% and 20%, there were full RBC volume recoveries within 120 min, RVI was partial at SO2 values of 45% and 55%, and RVI was absent at a SO2 of 100%. SO2 and P50 did not change significantly during RBC shrinkage and RVI. Thus, the up-concentration of cellular haemoglobin and organic phosphates in hyperosmotically shrunken RBCs had minimal influence on blood O2 transporting properties. The degree of cell shrinkage and time needed for RVI were positively correlated with the magnitude of the rise in extracellular osmolality. The RVI proceeded via elevation of cellular [Na+], [Cl-], and to some extent also [K+]. Cell volume regulatory mechanisms are only needed to correct minor volume disturbances in vivo, because changes in extracellular osmolality were limited by an efficient osmotic regulation at the epithelial interface between extracellular compartment and environment.
AB - Blood respiratory, acid-base, and ionic changes in response to hyperosmotic shock were studied in vivo and in vitro in the European flounder. One primary aim was to evaluate regulatory changes in red blood cell (RBC) volume and its interrelationship with blood O2 transporting properties. An acute increase in the ambient salinity from 10 to 30 ppt caused small but significant increases in extracellular osmolality (<20 mosM kg-1), [Na+], and [Cl-], which were corrected within 48 h. RBC volume was not significantly changed 3 h after the in vivo exposure to elevated salinity. A small metabolic acidosis was fully developed within 3 h, and this acidosis seemed responsible for a modest decrease in blood O2 affinity (i.e., increased P50-O2 tension at 50% O2 saturation). RBC organic phosphates were unchanged. In vitro elevation of whole blood extracellular osmolality by 60 mosM kg-1 caused immediate RBC shrinkage. The subsequent regulatory volume increase (RVI) showed a graded dependency on blood O2 saturation (SO2). At SO2 values of 0% and 20%, there were full RBC volume recoveries within 120 min, RVI was partial at SO2 values of 45% and 55%, and RVI was absent at a SO2 of 100%. SO2 and P50 did not change significantly during RBC shrinkage and RVI. Thus, the up-concentration of cellular haemoglobin and organic phosphates in hyperosmotically shrunken RBCs had minimal influence on blood O2 transporting properties. The degree of cell shrinkage and time needed for RVI were positively correlated with the magnitude of the rise in extracellular osmolality. The RVI proceeded via elevation of cellular [Na+], [Cl-], and to some extent also [K+]. Cell volume regulatory mechanisms are only needed to correct minor volume disturbances in vivo, because changes in extracellular osmolality were limited by an efficient osmotic regulation at the epithelial interface between extracellular compartment and environment.
KW - Erythrocyte
KW - Hyperosmotic shrinkage
KW - Oxygen affinity
KW - Oxygenation-dependent RVI
KW - Salinity challenge
KW - Volume regulation
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U2 - 10.1016/S0022-0981(02)00210-1
DO - 10.1016/S0022-0981(02)00210-1
M3 - Article
AN - SCOPUS:0037025864
VL - 274
SP - 159
EP - 174
JO - Journal of Experimental Marine Biology and Ecology
JF - Journal of Experimental Marine Biology and Ecology
SN - 0022-0981
IS - 2
ER -