J. F. SPANN, JR. AND G. M. LEMOLE 
155 
tion. You're quite right. The ventricle dilates in- 
j stantaneously, or virtually so. 
Dr. Hawthorne: The first thing that hap- 
pens is you have a volume v^hich can't get out. 
The pressure problem comes after the fact. To 
my knowledge the main problem is how do we 
get a preparation where pure pressure overload 
exists; so far none exists, 
j Dr. Spann : What do you call a volume over- 
! load? Diastolic volume is certainly up, but the 
stroke volume in these animals is normal, unlike 
a shunt. 
Dr. Hawthorne : Well, a pure volume over- 
load would imply that you stressed the resting 
sarcomere length out beyond 2.2 microns if you 
are thinking in terms of contractile elements. 
H. L. Brooks, University of Chicago: I be- 
came interested in the same problem, particular- 
ly in the acute right ventricular stress overload, 
as in a pulmonary embolus, and I wondered if 
you had looked at left ventricular dynamics as 
an explanation for the increased hydroxy proline 
levels which you noticed in the left ventricular 
free wall? If so, is there some mechanism to 
explain these increased levels' involvement of 
the left ventricle? 
Dr. Spann: No, we have no data at all in 
terms of instantaneous length and shortening 
and V-max on the left ventricle. The only facts 
we have on the left ventricle are the overall he- 
modynamics, i.e., the fact that the cardiac output 
was normal, that by implication the con- 
striction is over on the pulmonary artery and 
that the left ventricle does not hypertrophy. I 
also wish to point out that the norepinephrine 
changes were striking in the left ventricle. 
They were even more pronounced than the 
hydroxyproline changes on a percentage basis. 
This has, of course, been observed by others. 
Dr. Charles Chidsey first observed it in the dog 
when using the Barger preparation. 
