Acidosis, hypoxia and stress hormone release in response to one‐minute inhalation of 80% CO2 in swine


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The study pertains to a series of investigations on the effects of CO2 inhalation as used for pre‐slaughter anaesthesia in swine. Acid/base parameters, blood oxygen tension, plasma Na, K, Ca and stress hormone concentrations were monitored in Yorkshire swine before, during, and for 10 min after the animals were descended for 1 min into 80% CO2 in air. Severe respiratory acidosis (Paco2˜ 50 kPa, arterial pH ˜ 6.6) and hypoxia (Pao2˜ 4 kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2˜ 17 kPa, pH 7.1, Pvo2˜ 4 kPa). Readjustment to PaCO2˜ 11 kPa, arterial pH 7.2, and Pao2˜ 13 kPa had occurred at 1 min post CO2. Four minutes later the respiratory acidosis had become converted into metabolic acidosis subjected to partial respiratory compensation (arterial pH 7.3 in the presence of moderate hypocapnia and hyperoxaemia). The cause of this metabolic acidosis (present also at 10 min post CO2) was apparently hypoxia‐induced anaerobic metabolism (= lactic acid production). Apparently due to hydrogen ion transport into the cells in exchange for other cations, hyperkalaemia (K˜ 6.6 mmol 1‐l), and a 7 mmol 1‐1 increase in plasma Na had developed at 1.5 min later. The CO2 inhalation did not change the total plasma Ca significantly. The transport of the swine from the stable to the immediate pre‐experimental situation induced a 3‐fold increase in plasma Cortisol concentration (PC, to ˜ 130 mmol 1‐1). No further increase in PC occurred in response to the CO2 inhalation. It indicates that no additional emotional strain was imposed upon the animals during the CO2 exposure. Another possibility is that a maximal secretion of Cortisol was here reached already before the descent into the CO2. The transport procedure caused only minor increases in plasma adrenalin (A) and noradrenaline (NA). However, during the CO2 exposure plasma A and NA exhibited 15‐ and 50‐fold rises, respectively (to 3.5 and 22 mmol l‐1, respectively). The main cause of the A/NA elevation seems to have been the severe respiratory acidosis.

Sidor (från-till)223-231
TidskriftActa Physiologica Scandinavica
StatusPublished - 1988
Externt publiceradJa


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