In vivo myocyte sodium activity and concentration during hemorrhagic shock

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

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 (α(Na)(i)) 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 ~ 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, a(Na)(i) 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 a(Na)(i) 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 could account for the fall of the resting membrane potentials. This is the first direct in vivo measurement of a(Na) in cells during shock. The results support prior studies of Na+ flux and different intracellular Na+ compartments.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume258
Issue number3 27-3
StatePublished - 1990

Fingerprint

Hemorrhagic Shock
Membrane Potentials
Muscle Cells
Shock
Sodium
Skeletal Muscle
Hypovolemia
Microelectrodes
Acidosis
Blood Volume
Organelles
Anesthesia
Cell Membrane
Rabbits

Keywords

  • blood gases
  • blood pH
  • double-barreled sodium ion-selective microelectrode
  • intracellular water and extracellular water
  • membrane potential
  • plasma electrolyte
  • rabbit
  • skeletal muscle

ASJC Scopus subject areas

  • Physiology

Cite this

In vivo myocyte sodium activity and concentration during hemorrhagic shock. / Chiao, J. J C; Minei, J. P.; Shires, G. T.; Shires, G. T.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 258, No. 3 27-3, 1990.

Research output: Contribution to journalArticle

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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 (α(Na)(i)) 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 ~ 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, a(Na)(i) 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 a(Na)(i) 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 could account for the fall of the resting membrane potentials. This is the first direct in vivo measurement of a(Na) in cells during shock. The results support prior studies of Na+ flux and different intracellular Na+ compartments.",
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N2 - 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 (α(Na)(i)) 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 ~ 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, a(Na)(i) 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 a(Na)(i) 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 could account for the fall of the resting membrane potentials. This is the first direct in vivo measurement of a(Na) in cells during shock. The results support prior studies of Na+ flux and different intracellular Na+ compartments.

AB - 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 (α(Na)(i)) 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 ~ 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, a(Na)(i) 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 a(Na)(i) 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 could account for the fall of the resting membrane potentials. This is the first direct in vivo measurement of a(Na) in cells during shock. The results support prior studies of Na+ flux and different intracellular Na+ compartments.

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