W. B. HOOD, JR. AND J. C. NORMAN 
45 
200 
AORTIC 
PRESSURE 100 
( mm Hg ) 
L V 
JRE 
( mm Hg ) 
■ Glucagon 
PRESSURE ZO-'^A-f^ 
PA 
PRESSURE 2 0 
( mm Hg j 
LA 
PRESSURE 
( mm Hg ) 
HEART RATE 
( beats /mm J 
CARD/ AC OUTPUT 
( L /min ) 
2.8 
3,8 
Figure 5. — Tracings obtained during infusion of 
50/ig/Kg of glucagon into the pulmonary artery of 
an intact conscious dog one week after acute my- 
ocardial infarction. There is a decline in the initially 
elevated left atrial (LA) pressure, and an increase in 
heart rate and cardiac output following glucagon in- 
fusion. Similar results were observed after glucagon 
infusion in the acute phase of infarction. LV = Left 
ventricular. PA = Pulmonary arterial. (By 
permission.") 
ing the role that inotropic agents may play in 
increasing myocardial oxygen consumption and 
increasing damage in acutely infarcted myo- 
cardium.2- Evidently, this latter phenomenon 
may not exist when left ventricular failure 
is present and when the inotropic agent simul- 
taneously reduces ventricular filling pressure 
and volume. 
This canine preparation has also been tested 
with one intervention directed toward the prob- 
lem of salvaging myocardial cells around the 
margins of the infarct from ischemic damage, 
namely, hyperbaric oxygenation. This inter- 
vention was found to be without effect upon he- 
modynamic abnormalities even when applied at 
a time when ischemic damage was potentially 
reversible. The preparation seems to be suitable 
for testing other such interventions, including 
CONTROL 
ACUTE M.l. HEALING M.I. 
LVEDP 
(mm Hg) 
20- P<0.0 1 
I 0 
20 - 
MYOCARDIAL O2 
CONSUMPTION 
(ml/IOOgLV/minI 
p<0.02 
oi—i- 
p>0.8 
J_l I L 
p>0.5 
GLUCAGON; WITHOUT WITH WITHOUT WITH WITHOUT WITH 
getics. In one study, the observation was 
made that glucagon-induced inotropy after in- 
farction was not accompanied by an increase in 
myocardial oxygen consumption (Figure 6). 
Presumably this was due to the coincident low- 
ering of left ventricular end-diastolic pressure 
and volume, resulting in diminished wall stress 
and myocardial oxygen requirement, thus coun- 
terbalancing the increased oxygen requirement 
of increased inotropy. These observations are of 
interest in view of the current debate concern- 
FiGURE 6. — Changes in left ventricular end-diastolic 
pressure (LVEDP) and myocardial oxygen con- 
sumption in unanesthetized dogs studied in the con- 
trol state and one hour after myocardial infarction 
(acute MI-8 dogs), and again one week later (heal- 
ing MI-5 dogs). Values before and 13 minutes after 
administration of 50 /ug/Kg of glucagon are shown. 
Bars show mean ± SEM. In the control state 
LVEDP declined slightly but significantly after glu- 
cagon; oxygen consumption increased significantly. 
In acute and healing MI LVEDP declined substan- 
tially from the initially elevated values, while my- 
ocardial oxygen consumption did not increase signifi- 
cantly. See text for discussion. (By permission.") 
