Acidosis, hypoxia and stress hormone release in response to one-minute inhalation of 80% CO2 in swine.
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 approximately 50 kPa, arterial pH approximately 6.6) and hypoxia (PaO2 approximately 4kPa) had developed after 45 s of the CO2 inhalation. The corresponding changes in venous blood were less drastic (PvCO2 approximately 17 kPa, pH 7.1, PvO2 approximately 4 kPa). Readjustment to PaCO2 approximately II kPa, arterial pH 7.2, and PaO2 approximately 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 approximately 6.6 mmol l-1), and a 7 mmol l-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 approximately 130 mmol l-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.(ABSTRACT TRUNCATED AT 250 WORDS)
Forslid
A
A
Department of Physiology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden.
Augustinsson
O
O
D000142:Acidosis, Respiratory / Q000139:chemically induced*; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D002245:Carbon Dioxide / Q000008:administration & dosage* / Q000097:blood; D004573:Electrolytes / Q000097:blood; D004837:Epinephrine / Q000097:blood*; D006854:Hydrocortisone / Q000097:blood*; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000139:chemically induced*; D009638:Norepinephrine / Q000097:blood*; D010313:Partial Pressure; D013552:Swine; D013997:Time Factors
D001786:Blood Glucose; D004573:Electrolytes; D002245:Carbon Dioxide; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine