176 
CARDIAC MODELS 
Table VI. — Published Data On Experimental Cardiogenic Shock 
Author 
Animals 
HR 
sv 
CO 
TPR 
LVEDP 
Agress 
12 
146 
(±) 
-38% 
-39% 
± 
Goldfarb . 
18 
128 
(±4) 
—44% 
+61% 
(±21) 
23.6 
(±3) 
Lluch 
17 
174 ±7 
(+27%) 
—53% 
+41% 
7 
Cronin 
10 
140 
(-6%) 
-55% 
—58.5% 
+42% 
6.5 
Kuhn 
28 
126 
(-13%) 
—26.5% 
—35% 
± 
± 
7 
lis 
(±) 
—50% 
—50% 
+11% 
16 
= Not reported. 
± = No change. 
controllable and gracied reductions in CI, SI 
and MER at rest or during stress; (d) freedom 
from fatal arrhythmias to permit chronicity; 
and (e) appropriate, though oftentimes inade- 
quate, compensatory changes in the myocardium 
and coronary collateral bed. We believe this has 
been accomplished by Hood et al.^^-ss in their 
conscious dog preparation using single or mul- 
tiple vascular occluders and the subacute micro- 
sphere technique.^ 
SUMMARY 
The clinical spectrum of myocardial impair- 
ment or dysfunction seen with ischemic heart 
disease is quite broad and dependent on the 
time of observation in the overall course of the 
disease and the existing compensatory changes 
of the myocardium and coronary circulation. 
These factors are not only important in design- 
ing an experimental cardiac model but also in 
its overall assessment with various therapeutic 
interventions. Design criteria for shock and 
failure models following acute myocardial in- 
farction are presented and the current state of 
the art assessed. 
ACKNOWLEDGEMENT > 
Drs. Frank W. Hastings and T. Joseph 
Reeves, whose spirited and probing comments 
provided many creative insights during the 
course of the investigations which are herein 
reviewed, I gratefully acknowledge. Miss Susan 
Green is also acknowledged for her dedicated 
secretarial assistance. 
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2. Weber, K. T., Dennison, B. H., Fuqua, J, M., 
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