p. KEZDI, S. N. MISRA, R. K. KORDENAT AND T. J. SMITH 
73 
number (5) of patients in cardiogenic shock 
with good results. 
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DISCUSSION 
CHAIRMAN La Farge : Thank you, Dr. Kezdi. 
We have time for a brief discussion of this very 
provocative paper. 
P. SOMANI, Abbott Laboratories, North Chi- 
cago, 111. : You had a very good model and I'd 
like to see some of the data that you might have 
acquired but which you do not have at the mo- 
ment. For a good model, I think you have to 
show also that some of the drugs which are clin- 
ically used are effective in your models by im- 
proving the mortality rate. I have not seen this 
in this morning's presentation. I'd appreciate 
your comment on that issue. 
Dr. Kezdi : Very good. We had the mortality 
figures ; I even have a slide on the subject, but 
time is short. I indicated mortality with diben- 
zyline. In the combined norepinephrine and 
isoproterenol-treated animals, nine out of ten 
survived more than two days: obviously, the 
mercury erodes through the vessel wall after 
few days and you have to consider this when 
evaluating mortality. But taking 48 hours as a 
critical point, nine out of ten of these animals 
survived, which is 90% ; all other drugs resulted 
in a much lower survival rate. 
Lloyd G. Phillips, University of Minne- 
sota, Minneapolis, Minnesota: Dr. Kezdi, did 
you obtain any significant immediate mortality 
from the primary injection of mercury? 
Dr. Kezdi: Yes. 18% of the injected animals 
developed ventricular fibrillation. A very small 
number (2%) could be converted and we could 
continue the experiment. The overall total is 
about 75% of the injected animals which will 
live and develop a good standard model of 
cardiogenic shock. 
Dr. Somani: Dr. Kezdi, I was quite in- 
trigued by your results that the sympathetic 
amount of activity was not increased. Now the 
increase in sympathetic activity in any type of 
shock model is related to the time factor after 
your correction of the shock. For example, in 
hemorrhagic shock the sympathetic activity is 
initially very high but as the time goes by, the 
activity becomes very low. Did you find some- 
thing similar in your cardiac shock model ? 
Dr. Kezdi: We have not followed the activ- 
ity longer than five hours. But there is a differ- 
ence between the hemorrhagic shock and the 
cardiogenic shock model. In hemorrhagic shock 
you don't damage the heart initially at all and 
you have immediate baroceptor reflex compensa- 
tion. Therefore you have a marked increase of 
sympathy activity. I assume that in the cardio- 
genic shock model you have immediate stimula- 
tion of the Bezold-Jarish reflex. Later on they 
probably adapt but after a while the decreased 
sympathetic activity is probably due to other 
factors. One of these could be the stimulation 
of ventricular stretch receptors. Thus, sym- 
pathetic activity is down from the onset of 
myocardial infarction. 
Chairman : Dr. Kezdi, do you have measure- 
ments of coronary flow in response to this kind 
