CONNECTED WITH THE BEAT OF THE MAMMALIAN HEABT. 
175 
against tins })ossibility, which will he particularly misleading if the ti’ue hasal phase 
should happen to he weak or absent, but which may also confuse the i-eading of a 
normal ventricular variation. An illustration of this point is given in the note to 
Experiment 1. 
The origin of the excitatory ^^rocess can he experimentally determined. —Apart from 
the fact that true stimuli are capable of starting the excitatory process from any part 
of the ventricle, I have found that it is possible by local alteration of temperature to 
determine the origin of a series of contractions. An excised ventricle which has 
become quiescent can be made to resume rhythmic contractions by raising its tem¬ 
perature. If this be done in such a way that the apex is more warmed than the base, 
the diphasic variation at each contraction has directions denoting origin at apex; if in 
such a way that the base is more warmed than the apex, the directions of the diphasic 
variation indicate origin at base. 
Spontaneons modification ofi the ventricular variation. —It commonly happens that 
an original monophasic variation gradually gives place to a diphasic variation ; this 
change may be atti’ibuted to either of two causes : (1) to the subsidence of injury at 
the injured lead-off, or (2) to the development of injury at the normal lead-off. 
Fio-. 3. 
It appears to me probable that both these causes may j^lay a part in producing the 
effect in question ; as regards the first cause, we have in the Mammalian, as in the 
Batrachian heart, a rapid decline of the negativity manifested immediately after 
injury ; the negativity is doubtless an expression of chemical activity at and near the 
injured zone, or, in other words, of a state of continued excitation ; immediately after 
injury the degree of the alteration is such as to leave no margin for the manifestation 
of the excitatory effect (negativity) at the part, and an unbakniced negativity of any 
other normal part is witnessed in the shape of a monophasic variation when the organ 
contracts. The alteration is at first at a maximum, and gradually subsides until it 
leaves a maro-in of susceptibility within which excitatory eftects (negativity) can be 
evidenced, and now we witness a diphasic variation composed of the preponderant 
negativity of a normal part and of the recovering negativity of the injured part. It 
