Rôle of Afferent Nerves in Response of Vasomotor Center to Oxygen Deficiency. ∗

Abstract

Through numerous investigations it is known that the increased respiratory response to CO₂ is due less to its effect on peripheral receptors than on the respiratory center itself, whereas a similar response to oxygen deficiency occurs only when the carotid sinus nerves are intact. The removal of the afferent fibers by elimination of all known ”buffer nerves” results in a failure of respiration during O₂ deficiency (Selladurai and Wright, 1 Schmidt, 2 v. Euler and Liljestrand, 3 Smyth, 4 Gemmill and Reeves, 5 and Wright, 6 but cf. Dautrebande and Wegria 7 ). Under such circumstances the blood pressure reaction to O₂ deficiency may also be converted from the rise obtained in the intact animal to a fall (Selladurai and Wright, 1 and Brewer 8 . However, the question whether the organization of the vasomotor center is similar to that of the respiratory center can only be investigated when the respiration is kept constant and thereby secondary effects of a reduced respiratory volume eliminated.

Such studies were carried out on narcotized dogs (Na-barbital, Na-amytal, chloralosane) with pneumothorax and artificial respiration. O₂-N₂ gas mixtures (1.0 to 9.8% o₂) were prepared by means of flowmeters, analyzed and inhaled from Douglas bags for periods of from 1 to 3 minutes and the blood pressure effects were recorded. After the control reaction consisting of a rise in blood pressure was obtained both vagi were cut in the neck and both carotid sinus regions were denervated. Hereafter the same O₂-N₂ mixture was inhaled and invariably an immediate fall of blood pressure was observed which occured regularly no matter whether the blood pressure level was unchanged, higher or lower than under the control conditions.