PubMed Health⌕ Search

Biomedical subjects

G D Meier

Publications and source records attributed to G D Meier.

6 recordsLinked to original sources

Helical fibers in myocardium of dogs change their pitch as they contract.

We have investigated the dynamic relationship between fiber structure and deformation of the epicardium in the canine right ventricle. We have reconstructed this deformation as the motion undergone by groups of three radiopaque markers implanted close together in small epicardial regions. As reported earlier, this motion has a stretch and a rotation component. The stretch relates to shortening in the epicardial segment, whereas the rotation describes how this segment changes orientation during the heart cycle. If one postulates this segment as attached to a myocardial spiral, then one can interpret the systolic shortening of the ventricular axis as a compression of the spiral with decrease in pitch and the diastolic lengthening as an extension with increase in pitch. If one further postulates that the epicardial segment is attached to a right-hand spiral, then decreases in pitch imply local clockwise segment rotations, and increases, local counterclockwise rotations. From the motion of the implanted markers, we have found that a small segment ion the midfree wall of the right ventricle twists first locally clockwise as the ventricular axis shortens and later counterclockwise as the axis lengthens. We conclude that deformation of the epicardium is the result of a helical fiber arrangement that is characteristic of the endocardial half of the wall. Near the apex we observed the segment rotation to be reversed: counterclockwise during systole and clockwise during diastole. This observation implies a left-hand helix, which is the path of the apical epicardial fibers, suggesting that the endocardial half of the wall is no longer predominant here.

Animals↗

Contractile function in canine right ventricle.

Regional right ventricular (RV) motion was examined in six acutely instrumented dogs by implanting radiopaque markers in three regions of the free wall: the apex, the midventricle, and the outflow tract. These markers were filmed at the paced heart rate of 180 beats/min with a high-speed biplane X-ray system, and their motion was analyzed with a digital computer. Local deformation was separated into percent length changes in the two mutually perpendicular principal directions. The major component exhibited shortening along a path from apex to conus. (apex - 13.6%, midventricle -13.1%, conus -8.7%); the minor component exhibited small amounts of lengthening and some shortening (apex +4.7%, midventricle +1.8%, conus -0.5%). From these two measurements we calculated the peak RV free wall thickening (apex 13.6%, midventricle 14.1%, conus 10.9%). The experimental technique developed for this study was found to be suitable for the repeated analysis of intact ventricular performance in chronic animal studies. The results reveal that in systole the RV free wall undergoes a sequential contraction, which begins at the apex and ends in the conus.

Animals↗

Effects of hemodynamic alterations on wall motion in the canine right ventricle.

Regional right ventricular (RV) wall motion was analyzed in six closed-chest, anesthetized, paced dogs by measuring distances between chronically implanted radiopaque markers on RV free wall and septum. Normally, contraction started in the sinus region 25 ms before conus region. Highest velocities of shortening occurred in the conus region (2.42 +/- 0.33 lengths/s) and in septum-to-free-wall direction (2.56 +/- 0.40 l/s). Percent shortening for all regions was between 12% and 17%. The data indicate that the RV ejects blood by a uniform reduction in its free wall surface area and septal-to-free-wall distance. Reduced venous return decreased end-diastolic length, percent shortening, maximum velocity of shortening, and time to end-systolic length. RV pressure overload increased end-diastolic length and decreased percent shortening and maximum velocity of shortening. LV pressure overload led to a nonhomogeneous contraction pattern. Percent shortening and maximum velocity of shortening increased in sinal and conal transverse directions and decreased in sinal and conal longitudinal directions; these changes indicate a mechanical interaction between RV and LV.

Animals↗

Left ventricular effects on right ventricular developed pressure.

The possibility that left ventricular (LV) performance might affect right ventricular (RV) function through the myocardium was examined by using isolated, flow-perfused, paced rabbit hearts beating isovolumically. Reducing LV volume from its optimal volume to zero caused a 5.7% decrease (N = 10, P less than 0.001) in right ventricular developed pressure (RVDP). Ligating the anterior ventricular branches of the left coronary artery which in the rabbit supply the LV free wall resulted in an additional 9.3% decrease in RVDP (N = 5, P = 0.05) within 3 min of ligation. Finally, cutting the LV free wall from the atrioventricular orifice to the apex (thereby preventing any developed LV free wall force during systole) caused a 45% further decrease in RVDP (N = 2, P less than 0.02). Cineradiographic study showed that the alterations in RVDP resulting from changes in LV volume and coronary occlusion correlated significantly (N = 5, P less than 0.01) with the magnitude of septal bulging into the RV cavity during systole. The results indicate that alteration in LV free wall function and changes in LV volume can directly effect RVDP through the myocardium.

Animals↗