The forces generated within the musculature of the left ventricular wall

Abstract

Objectives: To test the hypothesis that two populations of myocardial fibres-fibres aligned parallel to the surfaces of the wall and an additional population of fibres that extend obliquely through the wall-when working in concert produce a dualistic, self stabilising arrangement.

Methods: Assessment of tensile forces in the walls of seven porcine hearts by using needle probes. Ventricular diameter was measured with microsonometry and the intracavitary pressure through a fluid filled catheter. Positive inotropism was induced by dopamine, and negative inotropism by thiopental. The preload was raised by volume load and lowered by withdrawal of blood. Afterload was increased by inflation of a balloon in the aortic root. The anatomical orientation of the fibres was established subsequently in histological sections.

Results: The forces in the fibres parallel to the surface decreased 20-35% during systolic shrinkage of the ventricle, during negative inotropism, and during ventricular unloading. They increased 10-30% on positive inotropic stimulation and with augmentation in preload and afterload. The forces in the oblique transmural fibres increased 8-65% during systole, on positive inotropic medication, with an increase in afterload and during ventricular shrinkage, and decreased 36% on negative inotropic medication. There was a delay of up to 147 ms in the drop in activity during relaxation in the oblique transmural fibres.

Conclusion: Although the two populations of myocardial fibres are densely interwoven, it is possible to distinguish their functions with force probes. The delayed drop in force during relaxation in obliquely oriented fibres indicates that they are hindered in their shortening to an extent that parallels any increase in mural thickness. The transmural fibres, therefore, contribute to stiffening of the ventricular wall and hence to confining ventricular compliance.

Figure 1

Illustration showing the 2.5 mm thick needle force probe inserted between the myocardial fibres. Also shown is the main direction of the development of contractile force along the axial alignment of the myocardial fibres, along with the perpendicular force vector that acts on the flexible bar within the lateral window, measured by strain gauges mounted on the flexible bar. The fibres are spread during implantation of the probe. Some fibres slip into the lateral window, loading there on the flexible bar. Only those (bright) fibres that are curved around the flexible bar contribute to the signal measured, the innermost curved fibres more than the outer, less curved fibres. In the background are shown the myocardial fibres wrapping around the trunk of the needle probe. Spreading of the tissue is more important in this area than in the indentation of the window.

Figure 2

Continuous recording of left ventricular pressure, one force of the unloading type and one auxotonic force in the left ventricular wall, and left ventricular outer diameter during the withdrawal of 2 litres of blood within 15 minutes. Note the typical shapes of the unloading and auxotonic types of tensile forces. Note also that the auxotonic force increases while the ventricular diameter decreases.

Figure 3

Cross sections through two sites of implantation of force probes into the left ventricular wall. The left panel shows the alignment of the fibres running parallel to the epicardium. In this area, the measured signal was of the unloading type. The right panel, in contrast, shows fibres that take a strongly oblique and transmural course. A signal of the auxotonic type was measured at this site. Note that the zone of implantation in the right section from near the left ventricular base is situated beyond the mid-layers, whereas in the left section it is situated at the limits of the outer to the mid-third of the wall. The incidence of auxotonic signals is higher in the deeper than in the superficial layers.

Figure 4

Response of the diastolic (upper), systolic (middle), and developed (lower) tensile force of the unloading (left) and auxotonic (right) type (1) during inflation of the balloon in the aortic root, the addition of (2) 15 μg/min dobutamine (Dobu), (3) 200 μg thiopental, and (4) 1.5 (0.7) l of saline given intravenously within 15 minutes, and (5) fast withdrawal of the first 2 l of blood from the left atrium. Notice the significant changes in the averaged systolic auxotonic signal during inotropic interventions and the almost missing changes in the systolic auxotonic signal on withdrawal of volume. The differences in both signals are most significant in developed force. *p < 0.05; **p < 0.01.

Figure 5

Changes in the velocities in rise (upper) and drop (lower) of the unloading type (left) and auxotonic type (right) of tensile force (1) during an acute increase in left ventricular outflow resistance, addition of (2) 15 μg/min dobutamine (Dobu) and (3) 200 μg thiopental, both given intravenously, and (4) 1.5 (0.7) l saline given intravenously, and (5) withdrawal of the first 2 l of blood within 10 (23) minutes from the left atrium. Note the particularly significant response to inotropic interventions. *p < 0.05; **p < 0.01.

Figure 6

(A) Histogram of the duration of contractile activity versus slope in tensile force. The duration of activity is the time from the onset at the peak of the R wave until the corresponding level of tensile force has been reached at the end of systole. The duration of contractile activity was short in the unloading type of force (left) and long in the auxotonic type (right). The number of curves counted in the graph is the number of the measuring sites in all animals times four, since at each site measurements were made during two heart cycles, each at two extreme states of ventricular filling. (B) Systolic intervals from the peak of the R wave to the maximum velocity of rise in tensile force, the onset of fibre shortening, the end of fibre shortening, the maximum velocity of the drop in force during relaxation, and the end of activity when force reaches the same level as during the peak of the R wave. Note that only the duration of the last systolic interval in the auxotonic signal is significantly different from that in the unloading type of signal. *p < 0.01.