p. KEZDI, S. N. MISRA, R. K. KORDENAT AND T. J. SMITH 
67 
the animals with early death but this difference 
was only of borderline statistical significance. 
Cardiac output decreased markedly to about 
50% of the baseline in both groups, with the 
nonsurviving slightly lower at the end of five 
hours. The same was true for the stroke vol- 
ume. Peripheral resistence increased in both 
groups. The most significant variable which 
showed statistically significant difference after 
five hours of monitoring was the left ventricu- 
lar dP/dt with the animals surviving longer 
than 48 hours showing a tendency toward im- 
provement while the ones which died showing a 
continuous deterioration. This difference in 
dP/dt was not apparent in the initial phase of 
monitoring. Oxygen consumption, cardiac out- 
put and stroke volume paralleled this difference 
in dP/dt to a lesser degree. 
When the average infarct weight of the early 
expired and animals surviving more than 48 
hours was compared, it was found that the ex- 
pired dogs had 47.83 ± 13.44 grams while the 
survivors 30.75 ± 6.29 grams of infarct weight. 
This difference was statistically significant at 
the 1% level. The total heart weight was not 
different between the two groups. 
Thus, it appeared that initially no hemo- 
dynamically significant differences could be de- 
tected between the longer surviving and early 
expiring animals. After five hours of shock the 
left ventricular dP/dt, the stroke volume, left 
ventricular end-diastolic pressure, cardiac out- 
put and oxygen consumption, in this order, 
were the most significant prognostic differen- 
tiating signs. This difference in hemodynamic 
variables seems to relate clearly to the percent 
involvement of left ventricular free wall in the 
infarction and the early death of these animals 
was probably due to the greater degree of so 
called pump failure. These findings closely cor- 
respond with the findings of Lluch et al.* 
Study of Vagal Affe rents 
It has been long suspected that vagal affer- 
ents from the heart may play a role in the 
regulation of circulation during myocardial in- 
farction and cardiogenic shock. The organism 
relies in part on circulatory refiex mechanisms 
compensating for the hypotension, the decrease 
of stroke volume and cardiac output. The system- 
ic baroceptors play a major role in these reflexes. 
The question arose whether these compensatory 
mechanisms are always optimally working in a 
given shock state. If vagal afferents from the 
heart are activated during myocardial infarc- 
tion they may overcome the attempt by the bar- 
oceptors to compensate and may, in fact, act as 
a positive feedback mechanism. In addition to 
the hemodynamic measurements we have ex- 
posed the vagus nerves bilaterally and one 
aortic baroceptor nerve for nerve impulse record- 
ing. Postganglionic sympathetic activity was 
recorded from a renal nerve. The renal nerve 
was exposed by a posterior retroperitoneal ap- 
proach. The technique has been described pre- 
viously elsewhere.^ 
Following baseline recordings of cardiac out- 
put, blood pressures, aortic and sympathetic 
nerve activity cardiogenic shock was produced 
by mercury injection through previously placed 
coronary catheter. The trend of hemodynamics 
and of the nerve activity was then followed by 
repeated recordings. The usual hemodynamic 
changes with 50% decrease of cardiac output, 
blood pressure decrease and tachycardia devel- 
oped in these animals. Simultaneously with the 
decrease of the mean pressure, withdrawal of 
the aortic nerve activity occurred representing 
a general withdrawal of systemic baroceptor ac- 
tivity (Figure 5). It was expected that a reflex 
increase of sympathetic activity should occur. 
Contrary to this expectation sympathetic activ- 
ity also decreased, indicating that no maximal 
vasoconstriction occurred (Figure 6). Thus, the 
increase in peripheral resistence was probably 
due to the greater decrease of cardiac output 
than blood pressure (Figure 7). When, at this 
time, the vagus nerve was cut or cold blocked, 
while leaving the aortic and the carotid sinus 
nerves intact, an increase of sympathetic activ- 
ity could be demonstrated in most instances 
concommitently with an increase of systemic 
blood pressure, heart rate and cardiac output. 
Aortic nerve activity simultaneously increased 
as a result of increased mean pressure (Figures 
6 and 7). 
These findings clearly demonstrated that af- 
ferent impulses in the vagus, probably originat- 
ing in the heart, overcome the baroceptor with- 
