Acta Physiol Scand 1993, 149, 153-156

The influence of afterload on uniformity of

segment shortening in feline left ventricles.
Importance of cross-f ibre contraction

E. H E X E B E R G and S. B I R K E L A N D
Surgical Research Laboratory, Department of Surgery, Haukeland Hospital,
University of Bergen, Norway

HEXEBERG, E. & BIRKELAND, S. 1993. The influence of afterload on uniformity of

segment shortening in feline left ventricles. Importance of cross-fibre contraction. Acta
Physiol Scand 149, 153-156. Received 1 February 1993, accepted 13 May 1993.
ISSN 0001-6772. Surgical Research Laboratory, Department of Surgery, Haukeland
Hospital, University of Bergen, Norway.

Previous studies have shown that the combined increase of preload and afterload leads
to a more uniform wall contraction. As our previous information with a stable
afterloaded situation showed considerable increase of left ventricular end-diastolic
pressure, we have as yet no information of how afterload per se effects uniformity of
segment shortening. We therefore analysed maximal systolic shortening of cross-
oriented segments for three consecutive beats during abrupt elevation of afterload in 12
open-chest cats. Peak left ventricular systolic pressure increased during the three beats
from 154k 5 mmHg (mean SEM) to 167 5 mmHg and 186 k 5 mmHg. Left
ventricular end-diastolic pressure remained unchanged. Maximal systolic shortening
was reduced for both segments with increasing afterload, in longitudinal segment
(LONG) from 7 . 6 f l . l to 6.1+1.0% (P < 0.005), and more pronounced for
circumferential segments (CIRC) from 12.2k0.7 to 8.3*0.9% (P< 0.0005).
Uniformity of maximal systolic shortening, LONG/CIRC, increased from 0.63 k 0.08
in the first beat to 0.73 kO.10 and 0.82+0.12 in the following beats (P< 0.02). We
conclude that uniformity of contraction for cross-oriented segments in the anterior left
ventricular wall is increased during increased afterload. We propose that this can be
explained by reduction of the effect of cross-fibre contraction with increasing afterload.

Key words : afterload, myocardial contraction, sonomicrometry.

T h e degree of uniformity has been proposed as
a third modulator or regulatory mechanism of
myocardial function in addition to classical
loading conditions and inotropy (Brutsaert et al.
1984). In a previous study it was shown that
uniformity of local myocardial contraction mea-
sured as the ratio of maximal systolic shortening
for two cross-oriented segments in the anterior
left ventricular wall, increased following com-
bined preload and afterload increments
(Hexeberg et al. 1989). T h e stable afterloaded
Correspondence : E. Hexeberg, Surgical Research
Laboratory, Haukeland Hospital, N-5021 Bergen,
Norway.
situation was analysed as a situation with
increased preload. Shortening in the longitudinal
direction of the anterior left ventricular wall is
more influenced by changes in preload than
circumferential shortening. As our previous
information with an afterloaded situation showed
a great increase of left ventricular end-diastolic
pressure, we have, as yet, no information on how
afterload per se effects uniformity of segment
shortening. The non-uniformity related to low
preload levels can be understood to be related to
different initial force production during con-
traction (Hexeberg et al. 1991). T h i s difference
in force production is related to different
influence of preload on end-diastolic sarcomere
153
154 E . Hexeberg and S . Birkeland
Table 1. Haemodynamics

Beat 1 Beat 2 Beat 3 ANOVA

~~

LVSP (mmHg) 154+5 167 k 5* 186 f5*t P < 0.0005

LVEDP (mmHg) 6.5k1.0 6.5f1.0 6.9k1.0 n.s.
CIRC (%) 12.2f0.7 10.9k0.9 8.3+0.9*+ P < 0.0005
LONG (Yo) 7.6k1.1 7.4k1.0 6.1fl.0Xt P<0.005
LONG/CIRC 0.63f0.08 0.73f0.10 0.82f0.12* P < 0.02
Mean k SEM. LVSP = maximal left ventricular systolic pressure. LVEDP = left ventricular end-diastolic
pressure. CIRC = circumferential segment shortening. LONG = longitudinal segment shortening. ANOVA =
analysis of variance with repeated measurements. + P < 0.05 vs. first beat, t P c 0.05 vs. second beat.

lengths in inner and outer wall fibres. Afterload
will not effect the degree of uniformity related to
differences in sarcomere length at end-diastole
but will counteract the force produced by the
contracting fibres. Afterload may thus influence
the degree of uniformity of deformation at
another time during the contraction cycle. It is
not known how fibres in the wall interact during
contraction; whether the fibres contract in-
dependently of each other or whether contraction
of perpendicularly oriented fibres within the wall
influence fibre contraction (cross-fibre contrac-
tion). T o explore how afterload influences
uniformity of contraction we analysed how
abrupt increase of afterload with modest in-
fluence on preload affected uniformity of per-
formance for cross-oriented segments in the
anterior wall of the left ventricle. Abrupt
afterload increments during occlusion of the
descending aorta have been shown to result in
only a modest increase of end-diastolic pressure
(Zile et al. 1989).
METHODS
Twelve cats (2.8-4.8 kg) were anaesthetized with
pentobarbital (35 mg kg-'), tracheotomized and ven-
tilated with a positive pressure respirator (50% N,O,
47.5% 0, and 2.5% CO,). The protocol was ap-
proved by the Norwegian State Commission for
Experiments with Animals. Following thoracotomy a
micro-tip pressure catheter was inserted into the left
ventricle (for details in preparation see Hexeberg et al.
1989). Aortic blood flow was obtained from an
electromagnetic flowmeter probe on the ascending
aorta. An inflatable balloon catheter was introduced
into the descending aorta via the right femoral artery
for loading manipulations. Cross-oriented pairs of
ultrasound crystals were implanted into the left
anterior ventricular wall. The longitudinal segment
was oriented approximately 15" clockwise to a line
between mid-aorta and apex. The circumferential
segment was positioned in a perpendicular direction.
Recordings were obtained in end-expiration on a
multichannel oscillograph during a rapid manual
inflation of the aortic balloon. If the inflation
manoeuvre was unsuccessful due to arrythmia or
insufficient pressure elevation inflation was repeated
following a brief period of stabilization. Three beats
within the maximum of five consecutive beats were
included in the further analysis; the change in left
ventricular end-diastolic pressure (LVEDP) should
not exceed 2.5 mmHg and maximal left ventricular
pressure (LVSP) should increase at least 25 mmHg
for the three beats in any animal. End-diastole was
defined as the rapid upstroke of the left ventricular
pressure signal. End-systole was defined as end-
ejection and identified as the zero crossing of the
aortic flow signal. SL,,, was defined as the maximal
segment length occurring between end-diastole and
end-systole. SLn,,"was defined as the shortest segment
length during systole subsequent to SL,,,. Segment
shortening was analysed as maximal systolic short-
ening, ((SL,,,-SL,,,,)/SL,,.) 100%. The ratio
between segment shortening of longitudinal and
circumferential segments (LONG/CIRC) was calcu-
lated. Data were subjected to analysis of variance
(ANOVA) with repeated measurements (Wallenstein
et al. 1980) and the Newman-Keuls test for contrasts
(Zar 1984).
RESULTS
Table 1 presents haemodynamics and shortening
results for the twelve animals. LVSP increased
during aortic balloon inflation (P < O.OOW),
whereas LVEDP remained constant. Circum-
ferential segment shortening deteriorated with
increasing afterload from 12.2 f0.7?/, for the
first beat to 8.3+0.9% for the third beat
(P < 0.0005). Similarly longitudinal shortening
decreased from 7.6 & 1.1 to 6.1 f 1.Ooh
(P< 0.005). LONG/CIRC-ratio increased with
increasing afterload from 0.63 & 0.08 for the first
beat to 0.82k0.12 for the last beat (P< 0.02).
 Aferload and unlformity of segment shortening 155
End-dlrrtole End-ryrtole

Circumferential directions
Fig 1. Influence of cross-fibre contraction. A schematic illustration of the three-dimensional
behaviour of the left ventricular wall. Fibres (shaded) in circumferential and longitudinal
directions are shown during end-diastole and end-systole. Arrows indicate directions of force.

wall (Fox & Hutchins 1972), and the myocardial

DISCUSSION
fibres are interconnected by collagen fibres
If we assumed that each of the segments were (Factor & Robinson 1988). T h e myocardial
individually contracting papillary muscles we fibres are thus not likely to move independently
would expect the ‘weakest’ segment, longi- of each other from an anatomical point of view.
tudinal, to be most hampered by increased From analysis of deformation for different layers
afterload (Sonnenblick 1962). In contrast, the it is evident that the fibres do not move
opposite was found. T h e cross-oriented segments independently of each other as deformation
can thus not be regarded as individually con- depends more on segment orientation than depth
tracting fibres, and the two segments therefore within the myocardial wall (Fenton et al. 1978,
most likely reflect that fibres in different layers Waldman & Cove11 1987, Waldman et al. 1988).
influence shortening of each other. Such a concept of tethering implies that short-
How can this discrepancy between the ex- ening in one direction counteracts shortening in
pected changes and the observed changes be the perpendicular direction. This can be visual-
understood ? Different curvatures exist for the ized for two perpendicular fibres in end-diastole
longitudinal and circumferential segment, and and end-systole (Fig. 1). Contraction of the
wall stress is generally higher in the endocardial, strongest fibre (circumferential) hampers short-
longitudinally oriented, than epicardial, circum- ening of the weaker (longitudinal) fibre which
ferentially oriented, fibres (Wong & Rautaharju remains at an unchanged length during con-
1968, Yin 1981). An increased wall stress level traction. T h e figure shows an extreme situation
with increased afterload should predominantly with no shortening of the longitudinal fibre for
affect the longitudinal segment which is related the purpose of presenting the principle of cross-
to endocardial fibre function (Birkeland et al. fibre contraction. T h e longitudinal fibre thus
1992, Hexeberg et al. 1991, Hexeberg et al. contributes to wall thickening by not being
1992). As circumferential shortening was reduced elongated as compression in the circumferential
more compared with longitudinal shortening, direction is transformed into wall thickening. I n
changes in wall tension caused by geometrical such a model a fibre has to counteract both the
factors probably play a less important role in the afterload from the left ventricular pressure and
observed change of uniformity of deformation. the forces applied from cross-fibre contraction.
The fibres in the myocardium are woven Matsuzaki et al. (1992) found that thickening
together as a continuous three-dimensional of the inner half of the wall was reduced with
network with blood vessels running across the increasing afterload whereas outer half thick-
156 E . Hexeberg and S . Birkeland
ening remained unchanged. At first glance this
seems to be contradictory to our observation as
we relate longitudinal segment to performance of
endocardial fibres. However, thickening of the
inner half-layer can occur without any shortening
of endocardial fibres given cross-fibre contraction
from the outer half-layer. I f we assume a
cylinder-model with constant height of the
cylinder during contraction, i.e. constant endo-
cardial fibre length, contraction of outer half
(circumferential) fibres must result in more
inner half-layer compared to outer half-layer
thickening. Thus, increased afterload with re-
duced shortening almost necessarily leads to
more reduction of inner compared to outer wall
thickening. T h i s notion of increased endocardial
compared to epicardial half-layer thickening is in
agreement with the observation that systolic
thickening increases from subepicardium to
subendocardium (Gascho et al. 1990), and that
cross-fibre shortening exceeds shortening in the
fibre direction in the endocardial part of the wall
(Waldman et al. 1988).
We conclude that uniformity of contraction
for cross-oriented segments in the anterior left
ventricular wall is increased during increased
afterload. W e propose that this can be explained
by reduction of the effect of cross-fibre con-
traction with increasing afterload.
This study was made possible by support from the
Norwegian Council on Cardiovascular Diseases.
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