In vivo myocyte sodium activity and concentration during hemorrhagic shock

Abstract

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 (alpha Na) 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 approximately 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, alpha i(Na) 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 alpha i(Na) also indicates that the depolarization of resting membrane potentials during sustained severe hypovolemia was not caused by the increased [Na+]i. The increase in extracellular [K+] during shock could account for the fall of the resting membrane potentials.(ABSTRACT TRUNCATED AT 250 WORDS)