1888.] Effects of increased Arterial Pressure on the Heart. 287 



V. " On the Effects of Increased Arterial Pressure on the Mam- 

 malian Heart." By JOHN A. Mc William, M.D., Professor 

 of the Institutes of Medicine in the University of Aberdeen. 

 Communicated by Professor M. Foster, Sec. U.S. Received 

 May 30, 1888. 



The following is a short preliminary statement of some of the main 

 facts elicited in the course of a recent investigation. The experiments 

 were conducted on chloroformed cats. The thorax was laid open, 

 artificial respiration being maintained, and the action of the auricles 

 and ventricles was recorded by means of the graphic method. The 

 contraction of the heart in ordinary circumstances having been 

 observed and registered, the arterial pressure was raised by constrict- 

 ing or clamping the last part of the thoracic aorta — usually for a 

 period of 4 — 8 seconds. Clamping for longer periods was often 

 accompanied by convulsive movements of the animal. 



The results may be briefly summarised as follows : — 



They fall into one or other of two categories according as to whether 

 the medullary cardio-inhibitory mechanism is (I) functionally active 

 in controlling the heart's action, or is (II) incapable of affecting the 

 cardiac beat. The latter condition is one that may result from 

 various causes, such as (a) section of the vagus nerves or paralysis of 

 their function through the influence of drugs, &c. ; (6) depression or 

 paralysis of the medullary cardio-inhibitory centre, brought about by 

 drugs or by other causes. 



I. In the first-mentioned condition, when the cardio-inhibitory 

 mechanism is in a position to control the heart's action, a marked 

 rise of the arterial pressure (such as results from compression of the 

 descending aorta) causes, as Marey has shown, a slowing of the cardiac 

 rhythm. 



I find that the rise of blood-pressure also causes marked changes in 

 the contraction force of the cardiac muscle. For a short time (a few 

 seconds, 1, 2, 3, &c), after clamping of the descending aorta there 

 occurs an augmentation in the strength of the beat — especially of the 

 ventricular beat ; meanwhile the rhythm has become slower than 

 before (fig. 1). 



Then there occurs a more or less sudden change. The auricular 

 contractions undergo a striking diminution in force. They remain 

 enfeebled until the compression of the aorta has been discontinued 

 and the blood pressure has fallen; then they gradually recover, 

 though the process of recovery may not always begin at once (figs. 1 

 and 2). 



The changes in the vertricular action consequent upon closure of 



