Background: Postmortem findings of edema to the brain and lungs following water intoxication have been documented withserum sodium concentration of 108-mEq/L (216-mOsm/Kg), far lower than the physiological osmolality of 135 -145-mEq/L (275 – 295-mOsm/Kg). In this study, we investigatedthe effect and extent of low sodium, resulting from drinking too much water, on the erythrocyte membrane architecture.
Methods: Appropriately, collected whole blood wascentrifuge to separate plasma from red cells. The packed cellswere washed three times and then re-suspended to ~25% hematocrit in isotonicsolution. 50-μl of the 25% suspension was incubated insolution of various tonicity ranging from 290 to 65-mOsm/kg sodium chloride (NaCl). Following incubation, the supernatant and pellets were analyzed for hemoglobin content, respectively by spectrometry and western blotting techniques.
Results: Red cells hemolyzed in solution when sodium salt concentration dropped to less than 95- mEq/L (190-mOsm/Kg). Below 190-mOsm/Kg, membrane rupture was rapid -displaying an S-shaped “cooperativity” pattern similar to that of oxygen-hemoglobin binding curve. Complete (100%) red cell hemolysis occurred at ≤80-mEq/L (160-mOsm/Kg).Hemoglobin content was approximately 50% lower in cellsexposed to hypotonic compared to isotonic or hypertonic solutions.
Conclusion: The human red blood cellsshow more resilience to changes in osmolality compared to reported data from other cells such as the brain and hung. Erythrocytes ruptured in-vitro when osmolality fell below 190-mOsm/kg/kg, whereasedema to the brain and lungs from water intoxication led to death and with reported postmortem serum osmolality of 216-mOsm/kg/kg. Red cell remained intact at 216-mOsm/kg because of itsflexible membrane and cytoskeletal network of proteins
