Cardiovascular responses in apnoeic asphyxia: role of arterial chemoreceptors and the modification of their effects by a pulmonary vagal inflation reflex

摘要: 1. In the spontaneously breathing anaesthetized dog, systemic circulation was perfused at constant blood flow; there no pulmonary flow and arterial P(O2) P(CO2) were controlled independently by an extracorporeal isolated pump-perfused donor lung preparation. The carotid aortic bodies separately pressure with of same composition as circulation.2. Apnoeic asphyxia, produced stopping recipient animal's movements and, time, making perfusing chemoreceptors hypoxic hypercapnic reducing ventilation lungs, caused increase in vascular resistance.3. While still hypercapnic, withdrawal body ;drive' resulted a striking reduction resistance. Re-establishing chemoreceptor immediately increased resistance again.4. asphyxia carried out while continuously oxygenated normal had little or effect on resistance.5. vasoconstrictor response apnoeic reduced abolished re-establishing movements, this occurred absence changes chemoreceptors. This abolition vasoconstriction due to reflex.6. slowed rate beating atria excitation can be over-ridden inflation reflex arising from lungs.7. It is concluded that cardiovascular responses observed are due, least part, primary reflexes engendered hypoxia hypercapnia. appearance these is, however, dependent upon being (inflation) vagal reflex.