2 74 



RESPIRATION 



breathing had increased five times or more, but the circulation 

 had apparently not increased at all. The pulse, etc., were also 

 hardly affected. With a great excess of COg, however, the ve- 

 nous return to the right heart is evidently much increased. This 

 was first definitely observed by Yandell Henderson, who also 

 makes the, to me, interesting remark that he first noted the signs 

 of increased circulation rate on myself, while I was nearly over- 

 come by accumulation of CO2 in a mine-rescue apparatus, without 

 any deficiency of oxygen. ^^ Similarly, great deficiency of CO2, as 

 in forced breathing or excessive artificial respiration, will dim- 

 inish the circulation rate ; and it seemed probable that great in- 

 crease in the oxygen pressure in the tissues (though this is diflRcult 

 to produce except under the high atmospheric pressures referred 

 to in Chapter XII) would have a similar effect. 



That this effect is actually produced in man is indicated by the 

 results of quite recent experiments by Dautrebande and myself.-^* 

 We found that when pure oxygen was breathed, particularly under 

 a barometric pressure increased to two atmospheres, the breathing 

 increases, as shown by a fall in alveolar CO2 pressure, and there 

 is a simultaneous slowing of the pulse. This indicated a slowing 

 of circulation through the brain, such as would compensate for 

 the high oxygen pressure of the arterial blood. The slowing would 

 of course raise the pressure of CO2 in the brain, and thus increase 

 the breathing. It would also explain the fact that though oxygen 

 at two atmospheres pressure has a rapid poisonous action on the 

 lungs and other living tissues directly exposed to it (see Chapter 

 XII), there are no evident cerebral symptoms until oxygen at 

 much higher pressures is breathed. 



The responses involved in the chemical control of the venous 

 return to the right heart were found by Henderson and Harvey to 

 be peripheral, but independent of the vasomotor nerves and nerve 

 endings. In the "spinal" cat they found that slow injections of 

 adrenalin, and other prolonged vasomotor stimulations, cause a 

 maintained elevation of arterial pressure, but only an evanescent 

 rise of venous pressure. Ventilating the lungs with air rich in CO2 

 (with ample oxygen) has, on the contrary, in the absence of the 

 medullary vasomotor center, no appreciable direct effect upon 

 arterial pressure, but induces a gradual, sustained and large eleva- 

 tion of venous pressure. They note also that during this action 



"Yandell Henderson and Harvey, Ainer. Journ. of Physiol., XLVI, p. 533, 

 1918. 



"Dautrebande and Haldane, Journ. of Physiol., LV, p. 296, 1921. 



