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CARDIAC MODELS 
stimulation in each of the papillary muscles that 
we studied and they were potentiated in a per- 
centage similar to the normal muscle. For ex- 
ample, let us assume that the normal tension 
was 1. You paired stimulation and it went up to 
2. Of course, those are not actual figures. In the 
failure animal, it was 0.1 and would go up to 
0.2. So the percentage rise was identical. 
However, none of the positive inotropic inter- 
ventions such as paired stimulation, digitalis, 
epinephrine, and calcium added together, would 
bring the failing papillary performance up to 
the nonpotentiated baseline level of the normal 
papillary muscle under any circumstances. We 
could raise it, but not up to the normal level. 
Regarding the first part of your question, I 
am convinced, incidentally, that this is not the 
way to measure compliance. We haven't said 
much about this because I don't know what to 
make of it. They look stiffer but they don't 
measure. 
Chairman: In your opinion, what is the 
mechanism of the problem in question? I ask 
because I am wondering about the left ventricu- 
lar changes observed in the presence of the 
right ventricular. Is this a dominant left coro- 
nary system in the cat and if so, could there be 
some involvement of the adjacent free wall of 
the left ventricle to the septum which could be 
limiting the left ventricle by the massive hyper- 
trophy which you obtained? 
Dr. Spann: That is a possibility. I don't 
think so from the electron microscopic studies. 
The mitochondrial crista which, I believe, are 
fairly sensitive indicators of oxygen depriva- 
tion, are completely intact. There is no scar, no 
evidence of myocardium degradation. We 
looked at hundreds of sections of these and ob- 
tained no information whatsoever different 
from the normal. It was very discouraging. 
W. B. Hood, Boston City Hospital: Most of 
the isolated muscle data were normal on a 
cross-sectional area. When you followed the 
anatomy of the situation and compared muscle 
with muscle, was there a stage of failure where 
the hypertrophied muscle actually compensated 
for its overload in the isolated studies, that is if 
you considered the whole muscle function. 
Dr. Spann : We did not look, as Meerson did, 
for a hyperstage before depression. We did not 
cross section it by time in order to find that out. 
We did not have enough points to answer that 
thoroughly. Considering the tension developed 
by the right ventricle, at the working end-dias- 
tolic pressure before we bled them or infused 
them, then the tensions were comparable per 
unit across the sectional area. In other words, 
they were working at the same wall tension be- 
fore we intervened in the hypertrophy and fail- 
ure group as compared to normal. As for the 
papillary muscles, they were not comparable. 
Without correcting for the cross sectional area, 
the value would still be at least half normal, even 
when taking just the papillary muscle into con- 
sideration. This, however, poses problems since 
you can select a papillary muscle the size of 
your finger or the size of your thumb, depend- 
ing on which one you pull out of the right ven- 
tricle. Therefore you could not be sure how big 
it was before it hypertrophied. It might have 
been a tiny papillary muscle and I would not 
know which one of the normals to compare it to. 
E. W. Hawthorne, Howard University Col- 
lege of Medicine, Washington, D.C. : Dr. Spann, 
how soon after your banding did the right ven- 
tricular end-diastolic volume increase? I raise 
that question with reference to an earlier com- 
ment indicating that this was presumably a 
pure pressure overload experiment. 
Dr. Spann : The fact is, the moment you put 
the clip on the pulmonary artery the ventricular 
volume approximately doubled and it seemed 
to maintain a similar volume throughout the 
rest of the experiment. I'm guessing now when 
stating that it doubled. The ventricle does dilate 
quite strikingly and it seems to stay that way. 
But we did not examine them eight to twelve 
hours later. Perhaps there is a stage when they 
compensated, become normal in volume, and then 
increased later. I can't answer that. Some in the 
hypertrophy group were not dilated at all when 
open chest measurements were taken after sacri- 
ficing the animal. 
Chairman: Dr. Hawthorne's precise observ- 
ations leave me almost speechless. What I was 
trying to say, Dr. Hawthorne, was that this 
preparation was generated by a pressure over- 
load in contrast to the original Barger dog 
where tricuspid insufficiency as a volume load 
was used from the very beginning in combina- 
