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We investigated how pacing from different endocardial sites affects the left ventricular three-dimensional contraction pattern and performance in intact anesthetized dogs. We used data from the motion of radiopaque markers implanted in the left ventricular endocardium in an analysis based on the polar decomposition theorem to determine the left ventricle's three-dimensional principal directions and magnitudes of deformation, and its axis and angle of rotation during the cardiac cycle. This paper also derives a new procedure that permits statistical comparison of different left ventricular cavity deformation patterns. During normal sinus rhythm and pacing from the right atrium, left ventricular septum, left ventricular apex, and right ventricular apex, the principal directions of left ventricular deformation remained relatively fixed with respect to the left ventricle's anatomy, independent of heart rate and pacing site. These directions were oriented in septum-free wall, anterior-posterior, and apex-base directions. End-systolic pressure and volume did not vary significantly among pacing sites. End-diastolic volume varied significantly among pacing sites, with right ventricular apical pacing producing the smallest end-diastolic and stroke volume. These results reveal that beats produced by right ventricular apical pacing eject less blood compared with beats produced by right atrial, left ventricular septal, or left ventricular apical pacing.

Recent experiments using laser diffraction techniques to determine the time course and extent of sarcomere shortening in thin bundles of cardial tissue have given results which suggest that the velocity of sarcomere shortening in cardiac muscle is independent of the developed force (Nassar et al., 1974; Krueger and Pollack, 1975). However, the anatomical complexity of the intact tissue precludes a definite interpretation of the data, since the exact relationship between the force being borne by the total tissue to the force being borne by any observed group of sarcomeres is uncertain. The single frog atrial cell provides a simple cardiac preparation in which the relationship between sarcomere velocity and sarcomere force is well defined, since these cells are only 1-2 myofibrils wide. The purpose of the present investigation was to determine if sarcomere velocity in the single frog atrial cell is dependent on force by measuring the time course of sarcomere shortening in single cells under conditions in which the cell developed markedly different forces. The results presented in this paper give direct evidence that the velocity of sarcomere shortening in the single cardiac cell depends on the force being developed by the sarcomeres. Thus, cardiac sarcomeres have a type of force-velocity relationship, although the exact nature of this relationship could not be determined in these experiments.

We studied sarcomere performance in single isolated intact cardiac cells using techniques that allow direct measurement of sarcomere length and force. This investigation dealt primarily with sarcomere performance during twitch contractions under lightly loaded conditions. In such contractions, there was a significant portion of the contraction in which sarcomere shortening occurred at constant velocity over a significant range of sarcomere lengths. The constant velocity phase of shortening was followed by a phase of shortening in which sarcomere velocity decreased markedly. Both the velocity and extent of sarcomere shortening depended on the stimulus parameters used to excite the cell. With threshold stimulation, sarcomere velocities during the constant velocity phase of shortening ranged from 1 to 5.5 micron/sec in different cells and significant slowing of sarcomere shortening began at sarcomere lengths of 1.8-2.0 micron. In contrast, when cells were stimulated with a long duration stimulus (200 msec) of large current strength, sarcomere velocities during the constant velocity phase ranged from 6 to 12 micron/sec, and significant slowing did not occur until a sarcomere length of about 1.6 micron was reached. The threshold stimulus strength-stimulus duration relationship was determined on the single cell, and it was found to be of the type expected for a cell having an intact excitable membrane capable of generating an action potential when depolarized to a fixed voltage threshold. The data presented in this paper give direct evidence that the lightly loaded cardiac sarcomere has a velocity of shortening which depends on the level of contractile activation but is independent of sarcomere length at sarcomere lengths greater than about 1.6 micron.

In a preceding paper, we employed an initially spherical, modified membrane model of the infarcted ventricle to investigate the relation between ventricular function and both infarct size and infarct stiffness. In the present paper, we have applied the same model to a set of different questions, namely, the consequences of enhanced or depressed inotropic state within the noninfarcted myocardium. When infarcted ventricles containing up to 41% infarction are examined, stroke volume appears to be relatively insensitive to increases in inotropic state. However, stroke volume falls rapidly when inotropic state is depressed below 80% of normal. For the case of a ventricle with a large, weakly contracting segment which is not totally infarcted, stroke volume is impaired only when the contractility of the weak region is diminished below 50% of normal. Finally, the stress concentration around a region of infarction appears to be dependent more strongly on the inotropic state of the noninfarcted tissue than on the infarct size.

We studied sarcomere performance in single isolated intact frog atrial cells using techniques that allow direct measurement of sarcomere length and force. The purpose of this investigation was to determine whether length-dependent alterations in contractile activation occur in the single isolated cardiac cell. This was accomplished by determining the effect of initial sarcomere length on the time course of sarcomere shortening and force development during auxotonic twitch contractions. The results presented in this paper demonstrate that the velocity of sarcomere shortening, the rate of force development, and the magnitude of force development during auxotonic twitch contractions all increase as initial sarcomere length increases over the range of about 2 micrometers to greater than 3 micrometers. These results indicate that the level of contractile activation increases as initial sarcomere length increases. Also, results are presented that indicate that the rate of increase of contractile activation during a twitch contraction also increases as initial sarcomere length increases. These length-dependent effects on contractile activation in conjunction with the slow time course of contractile activation cause the force-velocity-length relationship to be time-dependent: i.e., the velocity of sarcomere shortening at a given sarcomere length and load depends on the time during the contraction when the sarcomere reaches that length. The results suggest that length-dependent alterations in contractile activation may play a major role in the improved contractile performance that accompanies an increase in initial sarcomere length in cardiac muscle.