368 Messrs. G. A. Buckmaster and J. A. Gardner. [Aug. 19, 



notice any cessation of respiration constituting a danger-point, such as is 

 generally found constituting an initial danger-point in chloroform narcosis. 



In experiments with re-etherisation after recovery from ether, the effects 

 of the drug on the lung ventilation are less marked, a state of things already 

 referred to in connection with chloroform. 



General Discussion of Results. 



With unimpeded respiration under anaesthesia by chloroform, given at a 

 slight positive pressure, the ventilation of the lung takes place at a lowered 

 level. Whatever may be the condition of the gas exchange between the 

 alveolar air and the blood, the total exchange of gases between the animal 

 and the atmosphere is diminished in amount, and this continues throughout 

 the whole period of anaesthesia. From our data it will be seen that during 

 chloroform narcosis (in which breathing does not stop) the lung ventilation 

 is diminished in the first three minutes by from 30 to 80 per cent., or on an 

 average about 60 per cent, of its original value, and by a similar amount 

 after prolonged anaesthesia. 



It is during this early period that the initial danger-point occurs, and an 

 entire cessation of the respiration may take place, which may result in death. 



A simple explanation of this cessation of breathing on administration of 

 chloroform after deep and rapid respiration may, we think, be found in the 

 carbon dioxide content of the blood. The hyperpnoea, prior to the admini- 

 stration of the anaesthetic, probably reduces the carbon dioxide content 

 below normal, so that, as Mosso, Miescher, Haldane and Priestley, and Yandell 

 Henderson* have pointed out, the chemical stimulus necessary to keep the 

 respiratory centre in activity is reduced. The effect of the anaesthetic would 

 be to reduce the excitability of the centre to the effect of the carbon dioxide, 

 so that the quantity of this gas, even after a minute or two of reduced 

 respiration consequent on the administration of the drug, would not be 

 sufficient to maintain respiration, which accordingly would cease. If this is 

 the case, the stoppage of respiration after administration of the drug would 

 obviously depend on two factors, viz., the alveolar ventilation prior to 

 anaesthesia and the strength of the anaesthetic. If the ventilation were 

 sufficient to reduce the carbon dioxide much below normal, and the anaesthetic 

 were strong enough, cessation of breathing would occur ; if either of these 

 factors were reduced in a less degree, the effects would vary from slowing of 

 respiration or temporary stopping to a scarcely appreciable change. In all 



* ' Amer. Journ. Physiol.,' 1908, vol. 21, p. 126 ; 1909, vol. 23, p. 345 ; 1909, vol. 24, 

 p. 66 ; 1910, vol. 25, pp. 310 and 385 ; 1910, vol. 26, p. 260. 



