394 



Dr. S. W. Patterson. The- Antagonistic 



in asphyxia and independent of inhibition ; and Mathison (19) found the cause 

 to be due to lack of oxygen rather than excess of C0 2 in the spinal animal ; 

 but observed that heart-block may occur with large doses of CO2 even in the 

 presence of sufficient oxygen. 



Summary and Discussion of Results. 



Eecent work on contraction of skeletal muscle has tended to establish 

 more and more the view that the phenomena of contraction can best be 

 described by reference to alterations of the surface energy of the muscle 

 elements, and the length of the muscle fibres is a measure of the surface 

 of action. In the heart the mean volume is the guide we have to the length 

 of the muscle fibres, and it has been shown (20) that the heart reacts to 

 increased work by increasing its mean volume, whether the increased 

 work is evoked by greater diastolic inflow or greater arterial resistance. 



It will be seen, from the results given above, that C0 2 in all doses 

 appears to have a depressant action on the functions of the heart ; the 

 contractile stress is developed more slowly, the heart taking a greater 

 mean volume to carry out its work, but if the CO2 is continued, the 

 observed output diminishes. Since the coronary circulation is unaltered 

 this indicates a diminution of total ventricular output, and the venous pres- 

 sure rises owing to the damming back of blood in the veins. 



Adding adrenalin to the blood circulating through a heart which is capable 

 of responding, causes increased rate of contraction and rate of development 

 of contractile stress ; the heart can develop the requisite tension more easily 

 and from a position of shorter initial length, so the mean heart volume is 

 shifted to the systolic side. Adrenalin seems to have a specific action in 

 mobilising the " contractile substance " and increasing the energy changes 

 taking place at the surface of the muscle fibres during contraction. The 

 result is that the ventricle contracts violently and the blood is expelled under 

 great pressure into the aorta. The coronary perfusion is greatly increased 

 and the nutrition of the heart improved. Eelaxation takes place rapidly, 

 and since there is no resistance to the inflowing blood the venous pressure 

 falls ; but the onset of the next systole comes so early that the filling of 

 the heart, and consequently the output per beat, are less than normal, but 

 the total output of the ventricle per minute is equal to or greater than 

 normal. 



With C0 2 and adrenalin combined in proper doses we still obtain greater 

 rate of contraction and relaxation, but the whole diastolic period is 

 lengthened ; thus there is time for greater filling, and there is increased 

 output per beat and per minute. This increased observed systemic output 



