Abstract
Changes in the arterial erythrocytic 2, 3-Diphosphoglycerate (2, 3-DPG) concentration in mature rabbits in which respiratory failure was induced were observed in relation to arterial blood gas values. Thirty nine adult rabbits were used.
Three experimental acute respiratory failure models were developed: 1) acute normoxemic hypocapnia or respiratory alkalosis, induced by non-rebreathing mechanical hyperventilation under room air inhalation for 24 hours, 2) acute normoxemic hypercapnia or respiratory acidosis, induced by non-rebreathing mechanical ventilation under hypercapnic mixed gas (8% CO2, 20% O2 and 72% N2) inhalation for 12 hours, 3) acute hypoxemia associated with normal arterial PCO2 and pH, induced by nonrebreathing mechanical ventilation under hypoxic mixed gas (10% O2 and 90% N2) inhalation for four hours.
The concentrations of 2, 3-DPG began to increase gradually at two hours in the normoxemic respiratory alkalosis group, while they began to decrease at half an hour in the normoxemic respiratory acidosis. The changes in the 2, 3-DPG concentration and those of the arterial PCO2 or pH in the first two hours in these conditions correlated significantly with each other.
In the hypoxemia associated with normal arterial PCO2 and pH, 2, 3-DPG concentrations slowly increased for four hours after exposure, but there was no obvious correlation between the 2, 3-DPG concentration and arterial Pot. in this condition
Two types of subchronic respiratory failure were designed as followed: 4) hypoxemic hypocapnia resulting from the continuous exposure to hypobaric hypoxia (10% O2) for 11 days, 5) the hypoxemia associated with hypercapnia resulting from diffuse interstitial pneumonitis which was induced by repeated intravenous injections of N-Methyl-N-Nitrosourethane for two weeks.
In these subchronic conditions, the concentrations of 2, 3-DPG increased dependent on continuous marked hypoxemia, regardless of changes of arterial PCO2 and pH, and there were significant correlations between changes in 2, 3-DPG concentrations and changes in arterial PO2 under marked hypoxemic conditions. On the other hand, the 2, 3-DPG concentrations were observed to be more closely related to PaCO2 than PaO2 under mild hypoxemia associated with hypercapnic acidosis.
These findings suggested that the concentration of 2, 3-DPG is dependant on changes of arterial PO2, PCO2 and pH, but that it is influenced more by arterial PCO2 and pH in the acute phase of the respiratory failure, when the concentration increases in proportion to long-term marked hypoxemia despite the presence of hypercapnic or acidosis.
