DOSAGE OF THE MAMMALIAN HEART BY CHLOROFORM 
Conclusion 
The conclusion seems unavoidable that the heart muscle rapidly takes up 
CHC1, offered to it in the vessels of its coronary system, and that the quantities it 
takes increase with increasing tension of the chloroform in the solution circulating 
through it. 
The osmotic pressure of CHC1 5 in a dilution of i in 100,000 of physio- 
logical saline is about 1*61 mm. Hg., at 37 0 C. This is the lowest chloroform 
tension we have worked with. With very strong solutions, such as 1 per .1,000 
toxic after effects complicate the simpler relationship which holds for moderate and 
weak solutions. 
Equilibrium is rapidly (e.g., in fifty seconds) established between the intra- 
muscular chloroform and the circulating or perfused chloroform. When that is 
established, further exhibition of the circulating chloroform leads to no further 
increase of chloroform paralysis of the tissue, provided the solution-tension 
of the circulating chloroform is not altered. Indeed, if that solution-tension is 
maintained, but not increased, there gradually ensues in the course of minutes (e.g., 
ten to twenty minutes) a distinct diminution of the cardiac depression. Should, 
however, the solution-tension be altered, alteration in the depth of chloroform 
paralysis ensues in the sense that if the tension of CHC1, is increased, corresponding 
aggravation of the paralysis of the tissue immediately follows, while if the tension- of 
the circulating CHC1, be lessened, the paralysis of the tissue is immediately 
correspondingly diminished. The speed and completeness with which this recovery 
from functional depression follows forthwith upon replacement of the chloroform 
containing fluid by fluid free from chloroform is a remarkable and characteristic 
feature of the action of chloroform on the heart in weak and moderate concentrations. 
It suggests that, in obedience to the direction of the gradient of osmotic pressures, 
the chloroform in the muscle passes back from the muscle into the fresh fluid supplied 
at zero chloroform pressure. In this respect the chloroform behaves as though it 
were in solution in the muscle. Can this drug poison the muscle without entering 
into chemical combination with its substance ? Does it act as an anti-katalysator 
on the ferment processes which lie at root of the normal functional activity of the 
contracting tissue of the heart ? 
As to the question of differences of susceptibility to chloroform of different 
individual hearts, our observations indicate that such differences do occur in cats' hearts. 
The differences have been especially obvious to us in our experiments with weak 
solutions. The degrees of the difference can be studied by references to the table of 
data appended to the report. 
