154 THE MECHANISM OF THE CIRCULATION. 



On excitation of the central end of an intercostal nerve, there occurred a 

 rise of aortic pressure followed by a fall, or a fall was obtained from 

 the first. The pressure in the pulmonary artery fell also, but not 

 proportionately. It is thus evident that the pulmonary circulation can 

 be affected to a certain extent by sensory stimulation of the chest wall. 

 In confirmation of Bradford and Dean's work, Franems-Franck * 

 obtained, by excitation of the central end of the anterior crural nerve, 

 a rise of pressure in the pulmonary artery and in the aorta, accom- 

 panied by a fall of pressure in the left auricle. On stimulation of 

 the central end of the splanchnic nerve, he recorded a maintained 

 rise of tension in the pulmonary artery, while the aortic pressure varied, 

 owing to the reflex excitation of the dilator as well as the constrictor 

 fibres which govern the splanchnic vascular system. 



Francois-Franck recorded the volume of one lobe of the lung by the 

 plethysmography method. A paradoxical result is obtained on plethys- 

 mography of the lung, since the organ does not diminish, but swells on 

 contraction of the arterioles. This is owing to the distension of the 

 large and extensile pulmonary arteries, in consequence of the increased 

 resistance to the out flow, and the continuance of the input from the 

 right heart. Excitation of the peripheral end of the vagus in the 

 atropinised animal was found by Bradford and Dean to have no effect on 

 the pressure in the pulmonary artery, and they were unable to find any 

 evidence of pulmonary vaso-dilator fibres in this or any other nerve. 



On stimulating the depressor nerve, both the aortic and the 

 pulmonary arterial pressures fall together. 



Among the points which become manifest in these experiments the follow- 

 ing are of especial interest : — 



1. The lesser circulation is independent of the systemic circulation, within 

 certain limits. Increased resistance to aortic flow does not immediately 

 produce a back effect in the pulmonary vascular system, but only when the 

 aortic tension has been maintained at a high level for a considerable period, and 

 when the ventricle becomes fatigued. The left heart then fails to keep up the 

 systolic output. Even when this happens, the lungs act as reservoirs for the 

 blood, and the pressure does not materially rise in the right heart till the back 

 effect has continued for some time. Finally, the output of the right heart is 

 affected, and the blood congests in the venous system. To grasp how back 

 effects are produced in the circulatory system is of the utmost importance for 

 the proper understanding of the pathology of the circulation. 



2, The pulmonary vascular system is undoubtedly innervated from the 

 upper thoracic nerve roots, and thus comes under the influence of the central 

 vasomotor mechanism. From the results of the experiments which have been 

 considered, it might be concluded that the vasomotor effects arc very small. 

 In the light, however, of Lichtheim and Landgraf's researches on the ligature 

 of the pulmonary arteries, this conclusion may be wrong. If ligature of three- 

 fourths of the arterial channels produces rib effect when the thorax is 

 opened and artificial respiration is maintained, we cannot expect that a 

 constriction of the arterioles should produce a very great result in Bradford 

 and Dean's experiments, since these authors worked with the thorax open, and 

 with the aid of artificial respiration. In the normal animal, the vasomotor 

 phenomena may be found to be somewhat more important, just as Landgraf 

 discovered that a great fall of aortic pressure and a rise of tension in the right 

 heart is produced when he ligatured one pulmonary artery without opening 

 the pleural cavity. 



1 Arch, dc jihysiol. norm, etpath., Paris, 1896, p. 184. 



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