J. p. SPANN, JR. AND G. M. LEMOLE 
151 
concentration of 10 molar of L-norepinephrine, 
the increment in isometric force averaged 1.47 
± 0.23 gms./mm. sq. in muscles from cats of 
the right ventricular hypertrophy and conges- 
tive heart failure groups, a value significantly 
greater than that observed in the normal mus- 
cles, 0.84 ± 0.2 gms./mm. sq. Thus, the dose re- 
sponse curve was shifted upward, signifying an 
increased response to norepinephrine; the ca- 
techolamine depleted cardiac muscle from the 
hypertrophied and failing heart is supersensi- 
tive to the positive inotropic effects of exogen- 
ous norepinephrine. 
Contractility in the Intact Ventricle 
Since the previously described investigations 
of contractile performance were carried out on 
isolated muscles only, under conditions quite 
different from those existing in the intact ani- 
mal, the contractile mechanics of the intact 
right ventricle of cats in which heart failure, 
produced as described before, were also studied. 
The protocol followed in these experiments was 
as follows : The hemodynamic status of each cat 
was determined by right heart catheterization, 
the chest was then opened and an isovolumic 
contraction was then produced by total occlu- 
sion of the pulmonary artery in the preceding 
diastole. Simultaneous measurement of the 
right ventricular pressure and the rate of pres- 
sure rise (dP/dt) allowed determination of 
the maximum velocity of shortening (Vn.ax) 
and the maximal isometric tension per muscle 
unit in the intact ventricle.^'^ ^s This allowed a de- 
scription of the mechanical performance of the 
heart muscle of the intact ventricle within a 
framework of the velocity of shortening, muscle 
length and tension and provided a quantitative 
description of the ventricular performance 
within a construct of muscle mechanics as it has 
been previously described in isolated papillary 
muscle. Furthermore, to study the two groups 
of hearts at comparable end-diastolic volumes, 
the animals with failing hearts were bled to de- 
crease the end-diastolic volume and the normal 
animals were infused to increase end-diastolic 
volume; the isovolumic contractions were re- 
peated at various points along the Frank-Star- 
Hng curve of each ventricle. In this manner, a 
segment of the length-tension curve could be de- 
scribed for each ventricle, in vivo. After the de- 
termination of ventricular function, the papillary 
muscles of these ventricles were removed 
through the tricuspid valve for study. The ven- 
tricular wall was left intact, and passive pres- 
sure volume curves were obtained in each right 
ventricle. 
The maximum velocity of shortening was 
markedly reduced in the ventricular muscle of 
the intact, failing heart and the whole force-ve- 
locity relationship was shifted downward and 
to the left in the failing ventricle, a finding ex- 
actly like that seen in the isolated papillary 
muscle. The maximum velocity of shortening 
(Vniax) in the intact ventricle, obtained by ex- 
trapolation, was depressed 40 percent below the 
normal value in both hypertrophied and failing 
hearts. The peak isovolumic ventricular wall 
tension at spontaneous end-diastolic volumes 
was only slightly reduced from normal in the 
animals with hypertrophy and failure ; whereas, 
the right ventricular end-diastolic tension and 
spontaneous end-diastolic volume was elevated 
to twice the normal value. The normalized right 
ventricular end-diastolic volume and circumfer- 
ence from which this spontaneous resting and 
active tension were recorded Avere significantly 
elevated from the normal value in these 
animals. 
When the length-tension curves were ob- 
tained by manipulation of end-diastolic volume 
in the contracting right ventricles of the failing 
and normal hearts, it could be seen that the in- 
tact, failing ventricle, like the failing papillary 
muscle, is operating along an ascending limb of 
a generally depressed length active tension 
curve and not along the descending limb of a 
normal curve. In fact, when comparisons were 
made at similar end-diastolic normalized cir- 
cumferences, active tension was reduced to one 
half of the normal value in both hypertrophied 
and failing hearts. By operating to the right 
along its depressed length-tension curve, the 
failing ventricle can compensate, at the expense 
of increased end-diastolic volume, pressure and 
tension, and can maintain and even exceed the 
isometric tension usually developed by the nor- 
mal ventricle at its smaller end-diastolic 
volume. The cardiac output was often normal 
