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Arterial blood gases and acid-base balance were measured in adult rats using a cannula implanted in the aortic arch. These measurements were performed both in awake, unrestrained animals and in animals submitted to various circumstances i.e. (a) different diet: high and low sodium chloride intake, (b) anesthesia by pentobarbital or inactine and, (c) repeated blood sampling with concomitant replacement with the same volume of blood. For each group investigated the [HCO3 -]a vs. PaCO2, [H+] vs. PaCO2, PaCO2 vs. PaO2 relationships were determined. The values obtained (m +/- SD) from awake, unrestrained adult rats were respectively 7.47 +/- 0.02 for arterial pH, 34.5 +/- 3.0 Torr for PaCO2 and 90 +/- 5.5 Torr for PaO2; the calculated [HCO3 -]a concentration was 25.5 +/- 1.5 mmol . 1-1. The present results indicate that plasma bicarbonate concentration, within normal range, highly depends on the prevailing resting level of PaCO2 (n = 202; r = 0.82; P less than 10(-3)). In addition, the PaCO2 versus PaO2 relationship was highly statistically significant (n = 202; r = -0.43; P less than 10(-3). In the other experimental groups of rats, these relationships were virtually the same as above although mean values (+/- SD) for PaCO2, PaO2, pHa and [HCO3 -]a might vary with the group investigated. The mean value for whole pHi, obtained by the DMO method, reached 6.81 for pHa = 7.47 and was not correlated to PaCO2 level in normal conditions. The present data argue for the existence of a respiratory component mediating individual acid-base variations in a normal population of rats. Arterial carbon dioxide partial pressure, by determining bicarbonate ions reabsorption rate, would ensure pH regulation under normal circumstances.

The influence of oxygenation level (oxyhaemoglobin saturation 0 or 100%) on the relationship between plasma pH and erythrocyte pH was studied, in vitro, in normal human blood submitted to changes in carbon dioxide tension. Firstly, the pH of both true and separated erythrolysates were compared: for the former, tonometry was carried out on whole blood, before red cells lysis; for the latter, equilibration was performed on erythrolysate, pH values appeared different: at PCO2 congruent to 21 and 38 Torr, separated erythrolysate was more alkaline than true one, and at PCO2 congruent to 0 it was more acid. Therefore, to estimate pHe-pHi relationship, pHi was evaluated on true erythrolysate. When haemoglobin passed from the reduced to the completely oxygenated state, a significant decrease of both pHe and pHi was observed for a given PCO2 (respectively about 0.05 and 0.08 pH unit), and of pHi for a given pHe (about 0.04 pH unit). In either extra or intraerythrocyte fluid, the oxygen-linked pH difference was negatively correlated to PCO2.

The influence of temperature on the acid-base status of normal human blood was studied in closed systems (constant CCO2) and open systems (variable CCO2). pH-T coefficients of true plasma and erythrocytes in closed systems were similar to coefficients for water (dpH/dT = -0.017 U/degrees C at 25 degrees C). Between 26 degrees C and 42 degrees C there was no significant variation in the relative alkalinities [OH-]/[H+], the charge state of proteins in plasma and erythrocytes or the proton Donnan ration. The equations established enabled calculation of the pH of true plasma and erythrocytes and of blood PCO2 and temperature, using only one of these four parameters. Under open-system conditions, temperature was shown to cause a rise in the apparent buffer power of whole blood non-bicarbonate systems (28.8 and 34.8 mM.l-1.u-1 at 26 degrees C and 42 degrees C respectively). These results show (1) that erythrocytes in closed systems seem very well able to maintain proton distribution regardless of temperature fluctuations and (2) when blood temperature rises, it cannot be excluded that vital organs are better protected against respiratory disturbances.

The influence of temperature on the acid-base status of normal human deoxygenated whole blood was studied in open systems (variable total CO2 content). (1) When the temperature was raised from 26 degrees C to 42 degrees C, the apparent buffering value of deoxygenated whole blood for CO2 increased by 7% of its value at 26 degrees C; this increase was not statistically significant. (2) Comparing the present data with those obtained previously from oxygenated whole blood in the same temperature range (Castaing & Pocidalo, 1979) indicates that arterial and venous blood have slightly different buffering capacities for CO2 in the 26 to 42 degrees C temperature range. It also suggests that, at physiological SO2 levels (SO2 greater than or equal to 30%), the apparent buffering value of venous blood for CO2 would be increased by at least 10% of its value at 26 degrees C when the temperature is raised to 42 degrees C. (3) It is concluded that pH stability would be reduced upon CO2 uptake within tissues with a high metabolism and therefore a high temperature.