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Intracellular and extracellular acid-base changes in hemorrhagic shock
Respiration Physiology
|April 1, 1976
Summary
Hemorrhagic shock in dogs caused severe metabolic acidosis and increased lactate. Skeletal muscle maintained intracellular pH and bicarbonate, indicating a robust compensatory response to shock.
Area of Science:
- Physiology
- Pathophysiology
- Biochemistry
Background:
- Hemorrhagic shock leads to significant physiological derangements.
- Understanding acid-base balance during shock is crucial for treatment.
Purpose of the Study:
- To investigate the acid-base status and lactate levels in arterial and venous blood during hemorrhagic shock.
- To examine the intracellular acid-base balance in skeletal muscle during shock.
Main Methods:
- Inducing hemorrhagic shock in 21 dogs by reducing mean arterial blood pressure to 50 torr for two hours.
- Measuring blood lactate, PCO2, and pH in arterial and mixed venous blood.
- Analyzing intracellular lactate, pH, and bicarbonate in hind limb skeletal muscle.
Main Results:
- Blood lactate concentration increased sixfold during shock.
- Arterial blood showed metabolic acidosis partially compensated by respiratory alkalosis, while venous blood exhibited combined metabolic and respiratory acidosis.
- Skeletal muscle showed increased intracellular lactate and PCO2 but maintained intracellular pH and bicarbonate concentration.
Conclusions:
- Skeletal muscle demonstrates a significant capacity to maintain intracellular acid-base balance during hemorrhagic shock.
- This suggests an enhanced bicarbonate buffering system in muscle cells during severe acidosis.