BOWIE, PUROHIT, ADAMS, SOMAIAH, HAWTHORNE AND HINDS 
547 
Table IV. — Cardiovascular Measurements in Anesthetized Horses (Effect of Catecholamines)' 
Cardiac 
Ejection 
End-diastolic 
End-systolic 
Stroke 
Heait Rate 
Output 
Fraction 
Stroke Work 
Treatment 
Volume (ml) 
Volume (ml) 
Volume (ml) 
( beats/min ) 
(L/min) 
(% EDV) 
(Gm-meters) 
Control 
987.4 ± 70 
669.7 ± 74 
312.1 ± 23.2 
72 ± 6 
22.1 ± 2 
32.8 ± 2.7 
271.7 ± 21.5 
Epinephrine 
862.5 ± 95 
562.7 ± 92 
303.7 ± 32 
99 ± 6 
29.6 ± 3 
42.8 ± 4.6 
285.8 ± 9.3 
Control 
1056.4 ± 88 
425.9 ± 80 
320.4 ± 25.6 
68 ± 4 
21.6 ± 2 
31.7 ± 2.6 
276.5 ± 26.7 
Isoproterenol 
886.8 ± 73 
575.7 ± 83 
313.5 ± 43.3 
91 ± 5 
27.0 ± 3 
41.5 ± 5.0 
288.6 ± 37.5 
Control 
1032.8 ± 85 
712.6 ± 76 
316.8 ± 26.2 
68 ± 6 
20.0 ± 2 
31.9 ± 2.3 
271.3 ± 23.3 
Norepinephrine 
908.0 ± 93 
621.6 ± 80 
286.7 ± 30.3 
70 ± 5 
20.5 ± 2 
35.5 ± 3.1 
331.6 ± 39.6 
•Number of Horses used in each study are: Epinephrine 13, Isoproterenol 15 and Norepinephrine 16. 
without a significant change in stroke volume 
and stroke work. The mean increase in cardiac 
output v^as 7.5 liters/min vi^hich represented a 
33.94% increment. The left ventricular end- 
diastolic volume for the thirteen control horses 
ranged from 688.5 to 1,566.5 ml (mean EDV = 
987.4 ± 70 ml) ; v^hereas in the animals infused 
with epinephrine, the range was 413.5 to 
1,529.0 ml (mean EDV = 826.5 ± 95 ml). The 
end-systolic volume vi^as similarly higher in the 
control horses (mean ESV = 669.7 ± 74 ml) 
than in the epinephrine infused animals (mean 
ESV = 562 + 92 ml). The left ventricular 
stroke work v^^as slightly increased from control 
mean values of 271.5 ± 21.5 gm M/beat to 
285.8 ± 29.3 gm M/beat. The increment in the 
ejected fraction was 30.5% (from 32.8 ± 2.7 to 
42.8 ± 4.6). Thus both an increase in the ejec- 
tion fraction and the heart rate (37.5%) re- 
sulted in more complete systolic emptying. 
Isoproternol consistently produced similar 
directional changes in hemodynamics as did epi- 
nephrine. The mean left ventricular end-dias- 
tolic volume decreased from 1052.4 ± 88.5 ml 
to 886.8 =t 73.3 ml. A similar decrease in end- 
systolic volume (from 725.9 ± 80 to 575.7 ± 
83.7 ml) v^as seen. Stroke volume was not al- 
tered in any consistent fashion. The mean in- 
crease in heart rate v^^as 33.8% while the mean 
increase in cardiac output was 25.00%. The car- 
diac output was increased primarily through an 
increase in heart rate, while stroke volume gen- 
erally remained unchanged. 
The effects of norepinephrine differed mark- 
edly from those of epinephrine and isoproter- 
enol. The heart rate and cardiac output were 
not appreciably changed (Table IV). A slight 
decrease in both the end-diastolic and the end- 
systolic volumes was noted. Stroke volume was 
not increased above the control value. There 
was a slight increase in the ejection fraction 
from 31.9 ± 2.3% to 35.5 ±31%, but these in- 
crements were not consistent from one animal 
to another. There was a marked increase in the 
calculated stroke work index (22.15% ) . 
The action of epinephrine and isoproterenol 
on the equine heart consistantly resulted in an 
increased cardiac output, an increased heart 
rate, a decrease in end-diastolic volume, a de- 
crease in end-systolic volume, and an increase 
in the ejection fraction, with no appreciable 
change in either stroke volume or stroke work. 
Whereas, norepinephrine caused a slight de- 
crease in the end-diastolic volume, a decrease in 
the end-systolic volume but had no significant 
effect on heart rate, cardiac output or stroke 
volume. The ejection fraction was slightly in- 
creased and a marked increase in stroke work 
occurred. 
In our studies with horses, the major effect of 
epinephrine and isoproterenol was to increase 
the cardiac output by increasing the heart rate. 
James and Nadeau^^ have shown that the in- 
creased heart rate produced by isoproterenol is 
due to a direct action of this drug and its ana- 
logs on the sinus node. The infusion of epineph- 
rine and isoproterenol caused a decrease in 
the end-diastolic and end-systolic volumes along 
with an unchanged or slightly decreased stroke 
volume. This more complete ventricular empty- 
ing contributes in part to the elevation of car- 
diac output. The increased cardiac output seen 
in horses as the result of epinephrine infusion 
was 33.94% above the control value; whereas, 
in normal human subjects, the maximum rise in 
the cardiac output response is approximately 50 
percent larger than control values. Several 
studies have demonstrated that the cardiac out- 
put is consistently increased following the ad- 
ministration of epinephrine regardless of the 
species (man, dog, cat, rabbit, etc.).^''-^^ 
Dodge,-^ while studying the effects of isopro- 
