In vivo myocyte sodium activity and concentration during hemorrhagic shock

Chiao, J.J.; Minei, J.P.; Shires, G.T.; Shires, G.T.

American Journal of Physiology 258(3 Pt 2): R684-R689

1990


ISSN/ISBN: 0002-9513
PMID: 2316715
Document Number: 366808
The increase in intracellular Na+ concentration ([Na+]i) and H2O content and decrease in K+ concentration during hemorrhagic shock have been observed. However, the state of the increased [Na+]i has never been defined. In this investigation double-barreled Na+-selective microelectrodes were used to directly measure in vivo intracellular Na+ activity (aNai) in skeletal muscle cells during prolonged hemorrhagic shock. Resting membrane potential, [Na+]i, and H2O content were also studied concomitantly. Sustained hemorrhagic shock with metabolic acidosis was produced in 12 rabbits after removal of .apprx. 40% of estimated blood volume under light anesthesia. During prolonged shock, resting membrane potentials of skeletal muscle cells depolarized to -74.7 .+-. 1.7 mV from a base-line value of -92.6 .+-. 0.4 mV. [Na+]i increased to 14.22 .+-. 0.45 mmol/l from a base-line value of 11.50 .+-. 0.32 mmol/l. Intracellular H2O content also had a 2.2% increase, whereas levels of [K+]i and extracellular H2O content decreased significantly. However, aNai remained unchanged (4.07 .+-. 0.19 mmol/l in base line and 4.04 .+-. 0.20 mmol/l during shock). This makes the intracellular apparent activity coefficient for Na+ fall significantly from 0.356 in base line to 0.286 during shock. This result indicates that the extra Na+ that diffused into cell because of membrane dysfunction was bound to the fixed charges and/or compartmentalized into subcellular organelles. The unchanged aNai also indicated that the depolarization of resting membrane potentials during sustained severe hypovolemia was not caused by the increase [Na+]i. The increase in extracellular [K+] during shock could account for the fall of the resting membrane potentials. This is the first direct in vivo measurement of aNa in cells during shock. The results support prior studies of Na+ flux and different intracellular Na+ compartments.

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