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The effects of iv sodium bicarbonate (NaHCO3) and Carbicarb, an experimental buffer, were compared in a rat model of lactic acidosis induced by controlled hemorrhage and asphyxia. Although both NaHCO3 and Carbicarb were effective at alkalinizing the arterial blood in this model, NaHCO3 administration resulted in a rise in PaCO2 where Carbicarb did not (+9 +/- 2 vs. +2 +/- 2 torr at 2 min after infusion, p less than .01). Moreover, NaHCO3 resulted in a small decrease in intracellular brain pH as measured with P-31 nuclear magnetic resonance where Carbicarb afforded intracellular brain alkalinization (-0.03 +/- 0.01 vs. +0.08 +/- 0.02 pH units at 2 min, p less than .01). If these data are confirmed clinically, Carbicarb may offer advantages over NaHCO3 under conditions of fixed or limited ventilation.

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The effects of sodium bicarbonate and a bicarbonate-carbonate mixture on expired CO2 and the volume of distribution of bicarbonate were studied in eight anesthetized, paralyzed, and ventilated dogs made acidotic with HCl (5 mmol/kg) infused over 90 min. Both sodium bicarbonate and Carbicarb resulted in systemic alkalinization and comparable increases in the serum bicarbonate at 50 min (7.07 +/- 0.91 vs. 7.99 +/- 0.77, respectively; P = NS). Sodium bicarbonate infusion resulted in an increase in CO2 excretion that accounted for a fractional CO2 excretion of 0.20 +/- 0.09, whereas infusion of a bicarbonate-carbonate mixture resulted in a fractional CO2 excretion of -0.06 +/- 0.09 (P less than 0.01). The uncorrected volume of distribution of bicarbonate after sodium bicarbonate infusion was higher than that seen with the bicarbonate-carbonate mixture (0.60 +/- 0.07 vs. 0.34 +/- 0.03 l/kg; P less than 0.01). However, when the volume of bicarbonate distribution was corrected for expired CO2, there was no difference between treatment with sodium bicarbonate and the bicarbonate-carbonate mixture (0.44 +/- 0.07 vs. 0.38 +/- 0.04 l/kg; P = NS). These data demonstrate that, in this animal model of acidosis, sodium bicarbonate treatment of systemic acidosis is accompanied by a generation of a considerable amount of CO2, whereas treatment with a bicarbonate-carbonate mixture is not. This suggests that in states of impaired ventilation, a bicarbonate-carbonate mixture may offer more efficient systemic alkalinization and may be associated with less CO2 generation than sodium bicarbonate.

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Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar), a mixture formulated to avoid the objections to sodium bicarbonate therapy, has been compared with 1 mol/L NaHCO3 and 1 mol/L NaCl in the treatment of mixed respiratory and metabolic acidosis (pH 7.17) produced by asphyxia in rats. In clinically appropriate doses, intravenous NaHCO3 raised arterial pH only 0.03 unit, elevated arterial carbon dioxide pressure, and doubled lactate concentration. With Carbicarb, the pH rise was three times as great and the blood lactate level was unchanged. The new drug should be effective in treating the acidosis of cardiopulmonary failure without raising blood carbon dioxide pressure or lactate levels and at lower sodium doses than required for NaHCO3.

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Static pressure-volume curves were obtained from the upper and lower lobes of 5 excised human lungs. Comparison of the upper and lower lobe pressure-volume curves showed a small but significant difference. The upper lobes contained a greater percentage of total lobar capacity above approximately 80 per cent of the lung volume. It would thus appear that the difference in lobar elastic properties could influence ventilation distribution in normal humans.

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Capillaries of 7 and 12.5 mu diameter have been fabricated in silicone rubber. Whole blood treated with heparin has been perfused through these capillaries. Under flowing conditions, no clotting or other clumping effects have been observed and red cells appear to maintain a constant velocity. Oxygen transfer data to and from saline perfusing the 12.5 mu diameter capillaries have been obtained in order to determine how rapidly O2 will permeate the silicone rubber film. The data indicate that the capillaries simulate lung tissue oxygen exchange and will allow for the first time the experimental determination of oxygen exchange kinetics in flowing whole blood.

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The contour of a modified Fowler single-breath nitrogen washout was determined in 15 postmortem human lungs before and after static lung recoil had been increased by ventilation. Before ventilation, expiratory nitrogen versus volume curves exhibited the 4 phases similar to those seen in intact human lungs. The tests were repeated after ventilation with humidified air at room temperature for 3 hours at pleural pressures between -20 and +10 cm H2O at 15 breaths per min. After ventilation, the slope of the alveolar plateau (Phase III) decreased (P less than 0.01); the volume of Phase IV increased (P less than 0.01); and the closing capacity (Phase IV plus minimal volume) decreased (P less than 0.01). The data suggest that in the human lung the onset of Phase IV is not solely dependent on a pleural pressure gradient and that after ventilation, when static lung recoil is increased, the distribution of inspired gas in the excised human lung is more uniform, and at least some lung units empty more completely before zero transpulmonary pressure is reached.

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An abhesive or 'anti-glue' function for lung surfactant is proposed which is reconcilable with the known unfolding of alveolar walls at low lung volumes. The theory is developed based upon the fact that the work required to part wetted surfaces is directly proportional to the surface tension. Application of the concept of the spreading coefficient from surface physical chemistry S = gammata-(gamma lla + gamma lle), where the gamma's refer to the surface (interfacial) tensions among the tissue (t), air (a) and lining layer (ll) surface, is shown to explain qualitatively physiological data in lungs subjected to maneuvers with working fluids varying widely in surface tension and spreading properties.

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