xin RESPIRATORY RHYTHM 479 



of the placenta! circulation, the action of the external air is 

 required to start pulmonary respiration. 



No one can miss the analogy between foetal apnoea and that 

 which can be provoked on adult animals by artificial respiration 

 with the bellows. Both the one and the other are due to a certain 

 relation between the venosity of the blood and the excitability of 

 the respiratory centres ; -neither the one nor the other depends upun 

 an absolute reduction in the venosity of the blood, but rather upon 

 the low excitability of the respiratory centres. 



Under all circumstances in which there is an abnnrnuil 

 diminution in the excitability of the respiratory centres, or where 

 such conditions are produced experimentally, it is easy to obtain a 

 longer or shorter period of apnoea, by circulating through the 

 respiratory centres a blood that under ordinary conditions is 

 adequate for the maintenance of respiratory rhythm. 



In the rabbit, ligature of the two vertebral arteries and of one 

 carotid produces no conspicuous change in the respiratory 

 mechanism. But if the second carotid is compressed, with anvsl 

 of the cerebral circulation, there will at once be a marked dyspnoea, 

 followed by epileptiform convulsions,and then by a pronounced delay 

 in the respiratory rhythm, owing to the exhaustion of the centres 

 (Kussmanl and Tenner). If free course be then given to the How 

 of blood through the carotid, there will instantly be a period of 

 apnoea, due to the fact that the stimulation of the centres by the 

 venosity of the blood diminishes rapidly, while their excitability 

 is slowly re-established (Gad). 



A similar explanation holds good tor the apuoea produced 

 immediately after transfusion of blood (or even of a simple 

 isotonic solution of sodium chloride) in an animal which had 

 previously been bled copiously, so as to produce asphyxial dyspnoea, 

 and successive debilitation and retardation of respiratory move- 

 ments, owing to exhaustion of bulbar excitability (Gad). 



Similar to this is the apuoea from vigorous stimulation of unr 

 peripheral trunk of the vagus, which determines a prolonged 

 suspension of the beats of the heart. During this inhibition of 

 the cardiac systole arterial pressure falls enormously (as we have 

 seen), in consequence of which there is a marked diminution in 

 the arterial afflux to the vessels that irrigate the bulbar respiratory 

 centres. This determines so pronounced a dyspnoea as, on the one 

 hand, to subtract all the C0 2 from the blood in the pulmonary 

 vessels, and on the other, to produce a certain degree of fatigue in 

 the said centres. When the cardiac beats are re-established and 

 the pulmonary blood, strongly arterialised, flows on to irrigate the 

 brain, a characteristic suspension of the respiratory rhythm ensues, 

 because the blood is apuoeic in relation to the somewhat depressed 

 excitability of the centres (Meyer). Neither, then, is this any " true 

 apnoea " in Miescher's sense (due, i.e., to the positively apuoeic 



