116 
CARDIAC MODELS 
diac output increased at the expense of Group 
B, which included the remaining parts of the 
body. Fifteen minutes after infarction, the car- 
diac output was redistributed so that Group A 
received a 15% increase whereas Group B re- 
ceived 5% less. The changes 45 minutes after 
infarction were more marked with Group A or- 
gans receiving a 31% relative increase in car- 
diac output at the expense of an 11% decrease 
to Group B. 
Organ Blood Flow. Fifteen minutes after in- 
farction, blood flow to the cerebral hemispheres 
and to the heart was significantly reduced ; how- 
ever, flow to the right ventricle and right and 
left atrium, which had not been significantly re- 
duced 15 minutes after infarction, had returned 
to approximate control values 45 minutes after 
infarction. After both postinfarction micro- 
sphere injections, the blood flow was decreased 
to the remaining organs but not significantly to 
the liver and adrenal glands. 
DISCUSSION 
In our study, an extensive myocardial infarc- 
tion was produced after ligation of the left an- 
terior descending coronary artery similar to 
that observed in monkeys^*'^^'^'^ and in other 
species.22-24 fp^^g advantages of the closed- 
chest method in a nonanesthetized animal rec- 
ommend it over the open-chested, anesthetized 
preparations in which marked changes in the 
cardiovascular system^^ are sometimes super- 
imposed on the altered hemodynamics asso- 
ciated with positive pressure respiration. How- 
ever, "chair" restraining of nonanesthetized 
animals may be responsible for additional arti- 
facts not found, for example, in trained dogs in 
which myocardial infarction has been induced 
without anesthesia or restraining devices. ^^-^^ 
Although ventricular fibrillation has been 
studied after acute coronary occlusion,^^"^^ 
multiple episodes of ventricular fibrillation in 
the same animal have been rare. In our observa- 
tions, continuous electrocardiographic record- 
ings demonstrated the common occurrence of 
multiple episodes of ventricular fibrillation that 
were successfully terminated by the application 
of external D.C. electrical current. 
In most studies, sinus tachycardia has been 
observed after myocardial infarction 
however, in our monkeys no difference in the 
heart rate was observed before and after coro- 
nary ligation. Since the control heart rate was 
over 200 beats/min and much higher than that 
reported in isolated chair-restrained monkeys,^- 
our animals may have been under considerable 
sympathetic discharge and may not have reached 
basal values ; conditioning to the restraining 
chairs and more rigid isolation should probably 
be considered in planning future experiments. 
Several criteria have been proposed to define 
cardiogenic shock^^"^*' including: (1) a fall in 
mean arterial pressure of at least 30% with no 
recovery for at least 30 minutes; (2) ischemic 
changes in the ECG with no arrhythmias to ac- 
count for the fall in blood pressure; (3) a re- 
duction of 50% of the cardiac output. These cri- 
teria were met by those animals of Series I that 
died within 6Vi hours after myocardial infarc- 
tion and, consequently, the diagnosis of cardi- 
ogenic shock can probably be sustained in the 
Group I ("Dead") group in spite of a lack of 
progressive rise in heart rate and end diastolic 
left ventricular pressure. The discriminant 
analysis based on data obtained in the first 30 
minutes after infarction predicted the death or 
survival of the animals retrospectively. Thus, 
the present model may make possible studies on 
the therapy of cardiogenic shock that would be 
useful in managing this condition in man. 
The validity of studies on regional blood flows 
by the use of nuclide-labeled microspheres is 
well established.^^ No significant differences 
in the percentage distribution of cardiac out- 
put nor in individual organ flows were ob- 
served between monkeys that presumably died 
in cardiogenic shock and those that survived. 
Although the small number of observations and 
the large differences between animals may ac- 
count for this, another factor to consider in the 
interpretation of our findings is the probable 
high levels of sympathetic discharge evidenced 
by the tachycardia observed in the control peri- 
ods. A pattern commonly observed, though, was 
a redistribution of the cardiac output favoring 
the brain, heart, liver, and adrenals so that in 
spite of the actual reduction in organ blood 
flow, these organs were less affected than the 
remaining parts of the body. 
