Metabolic changes in human red cells during incubation of whole blood in vitro

1. Whole blood was incubated at 37°, while being dialysed against a large volume of iso-osmotic bicarbonate buffer, pH7·4. The buffer contained glucose and the essential inorganic components of blood plasma in proportion. 2. After 3hr. of incubation in vitro there is a loss of red-cell 2,3-diphosphoglycerate. 3. Isotope experiments show that this is due to an accelerated rate of destruction of this compound. 4. Simultaneously, there is an increase in the median of red-cell osmotic fragility. 5. After extended periods of incubation there is a decrease in the metabolic rate and a decrease in the ratio of the rates of lactate production to glucose consumption. 6. There is a continuous loss of total adenine nucleotide and, after the first 12hr. of incubation, a tendency for the intracellular Na⁺ and K⁺ to equilibrate with the plasma. 7. The standard deviation of red-cell osmotic fragility expressed among the red-cell population increases exponentially with the time of incubation.     

Kinetics of CO2 hydration in fermentors: pH and pressure effects

Fluctuations in pH and head-space pressure in a fermentor introduce temporary changes in off-gas CO(2) concentrations. These changes are quantified using a simple model based on kinetics of CO(2) hydration and gas-liquid mass transfer. The model is verified experimentally. An eigenvalue analysis of the model indicates that mass transfer is the parameter which controls the dynamics of CO(2) equilibration.     

Blood osmolality during in vivo changes of CO2 pressure

In 16 experiments male subjects, age 22.4 +/- 0.5 (SE) yr, inspired CO2 for 15 min (8% end-tidal CO2) or hyperventilated for 30 min (2.5% end-tidal CO2). Osmolality (Osm) and acid-base status of arterialized venous blood were determined at short intervals until 30 min after hypo- and hypercapnia, respectively. During hypocapnia [CO2 partial pressure (PCO2) -2.31 +/- 0.32 kPa (-17.4 Torr), pH + 0.19 units], Osm decreased by 3.9 +/- 0.3 mosmol/kg H2O; during hypercapnia [PCO2 + 2.10 +/- 0.28 kPa (+15.8 Torr), pH -0.12 units], Osm increased by 5.8 +/- 0.7 mosmol/kg H2O. Presentation of the data in Osm-PCO2 or Osm-pH diagrams yields hysteresis loops probably caused by exchange between blood and tissues. The dependence of Osm on PCO2 must result mainly from CO2 buffering and therefore from the formation of bicarbonate. In spite of the different buffer capacities in various body compartments, water exchange allows rapid restoration of osmotic equilibrium throughout the organism. Thus delta Osm/delta pH during a PCO2 jump largely depends on the mean buffer capacity of the whole body. The high estimated buffer value during hypercapnia (38 mmol/kg H2O) compared with hypocapnia (19 mmol/kg H2O) seems to result from very strong muscle buffering during moderate acidosis.     

CO2 dissociation curves of oxygenated whole blood obtained at rest and in exercise

In vitro CO2 dissociation curves for oxygenated whole blood were determined in 19 healthy male subjects at rest and during submaximal and maximal bicycle work. Hemoglobin concentration and blood lactate increased with increasing work load and accordingly buffer value of the whole blood increased while bicarbonate and Base Excess (BE) decreased, resulting in a downward shift of the CO2 dissociation curve during exercise. Despite the marked increase in buffer values of the blood, the slopes of the CO2 dissociation curves during exercise were found to be about the same as those obtained at rest. It was inferred that the increasing effect of increased buffer value, on the dissociation slope, was essentially compensated by the decreasing effect of diminished bicarbonate content. The advantages of this relatively constant CO2 dissociation slope for the indirect measurement of cardiac output by the Fick principle are discussed.