376 The Innervation of the Pulmonary Vessels. [Feb. 21, 



cardiac nerves in the branches of the ganglion stellatum and in the 

 annulus Vieussenii. As yet, however, we have not been able to 

 separate the pulmonary vaso-motor fibres from the accelerator fibres. 



The objection will of course be made that the effects are slight, 

 and no doubt they are, but when we consider that enormous changes 

 in the aortic pressure produce such extremely slight effects, it is clear 

 that, small as these effects are, they conclusively show that they are 

 dependent on the contraction of the pulmonary vessels, and not on 

 any passive effect from the slight rises in the aortic pressure. 



There seems no doubt that the vaso-constrictor mechanism of the 

 lungs is not very highly developed. It is impossible to get anything 

 like a doubling of pulmonary blood-pressure by any kind of nerve 

 excitation, although the systemic blood-pressure can easily be doubled 

 or even quadrupled. The amount of possible contraction of the 

 pulmonary arterioles is probably not nearly so great as that of the 

 systemic vessels, and this view is confirmed by the results of asphyxia 

 on the pulmonary circulation. 



Results of Asphyxia on the Pulmonary Circulation. 



In asphyxia both the aortic and the pulmonary blood-pressures 

 undergo a considerable rise, but the rise of pressure in the pulmonary 

 vessels lasts longer than that in the systemic, so that when the aortic 

 pressure is falling rapidly, the pulmonary may be at its highest point. 



The rise of pressure occurs synchronously in the two sets of vessels, 

 and the general course of the two curves is the same, except that the 

 pulmonary rise is more gradual than the aortic rise. As a rule, the 

 sudden and great elevations seen on the aortic blood-pressure curve 

 are not well seen on the pulmonary trace, but notwithstanding this, 

 the maximum rise of the pulmonary pressure may be very considerable, 

 e.g., it may be doubled. 



If, however, so large an effect as this is seen, the aortic pressure 

 will have undergone a very much greater relative rise, i.e., it will 

 have been quadrupled. 



The Traube curves, so well marked on the aortic blood-pressure 

 tracing, are but faintly marked in the case of the pulmonary artery, 

 and hence it is difficult to say whether the effects are direct or due 

 simply to passive reaction from the systemic circulation. It is probable, 

 however, that they are direct. 



The curious maintenance of the pulmonary pressure at such a 

 height as death approaches, when the aortic pressure has fallen 

 perhaps to half its previous height, is probably due to venous disten- 

 sion as much as to the increased peripheral resistance, but this is a 

 point we wish to investigate further. 



