June, 1952]
V.
RATHNASABAPHATY
AND
V.
ISWARI
155
minute. The auricles and the ventricles were beating in unision so far. After
this the ventricles were reduced in rate, while the auricles were maintaining their
normal rate. There was a single ventricular response for every two or more auricular
beats. After some time, complete block developed resulting in the ventricles having
their own rhythm and final arrest in diastole (Plate X).
The drug 1 : 2,00,000 concentration caused an initial increase, then a slowing
of the rate of the heart. By perfusion with normal Locke's solution at this stage,
apparently the normal rhythm of the heart was restored. But on repeating the
dose, heart block was produced in three minutes, the ventricles responding for
every two or more auricular beats only. The ventricles become irregular and were
arrested.
Similar changes were noticed even in the auricles with regular or irregular
intermissions. Finally, they were also arrested some time later than the ventricular
stand-still.
It was found that the chambers responded to mechanical stimuli as a pin prick
or pinching with fine forceps showing that the heart muscle was not dead and if
only adequate stimuli reach them, from the pace maker they would continue to
beat.
Contractility. In a physiological dose of gigantin, the heart was initially acce-
lerated but the amplitude was diminished. This phase was only transient. Soon
the rate was slowed while the amplitude was increased. The systolic contractions
were quicker and steeper whereas the relaxations were slower than normal. The
slowing was due mainly to a long rest in the normal pause. The increase in ampli-
tude was due to systole, the diastole being normal. These changes in the con-
tractility were observed in the auricles also but not to a marked degree as seen in
the case of the ventricle (Plate IX, Fig. c).
Cardiae out-put. In a physiological dose of the drug, the rate of the heart was
slowed but the amplitude and force of contraction were increased. The systolic
contraction was marked with no change in the diastole. The long pause in diastole
facilitated complete filling of the ventricle and the powerful systolic contractions
emptied the heart perfectly. Thus the out-put per beat may be said to be increased.
The slowing of the rate was thus compensated for by the increased pulse volume and
the out-put per minute might not be altered considerably by the drug.
Fixation and Cumulative effect. A dose of 0.05 mg. of gigantin given in the bulb
of the heart cannula slowed the heart and increased the force and contractions.
After about 30 minutes the heart was apparently normal, when a dose of 0.025
mg. was injected again into the heart cannula. This repetition produced not only a
slowing of the heart but also caused auriculo-ventricular heart block in about three
minutes. The ventricles responded once for every 2 or more auricular systole.
Finally due to complete block they developed ectopic beats and were arrested.
Thus a return of the heart to apparent normality was not an indication of the com-
plete elimination of the drug, but showed that some drug has been left behind and
were eliminated very slowly.
Electro-cardiogram of normal dogs taken in all the three leads after 0.05 mg.
per kg., of Gigantin intravenously showed only bradycardia.