The orientation of the muscle fiber bundles within the mammalian left ventricle was examined in a variety of mammals. The hearts were arrested in situ in animals with an intact thorax by means of an isotonic K+ solution perfused via the aorta and coronaries. The hearts were then fixed by formalin perfusion through the same vessels and the hearts embedded in gelatin. Serial sections were prepared perpendicular to the Apex-Valve axis. On close examination, the muscle fibers show the change in orientation from endocardium to epicardium previously described by others. In addition, the clefts and voids of the inner one-third to inner one-half of the left ventricular wall add another dimension to the fiber direction: the fiber bundles appear to take a curving course from the middle of the wall to the endocardial surface. This pattern was visible in all studied hearts. Speculations are made on the significance of this anatomic arrangement.

Sarcomere lengths were measured with an optical microscope at five sites through the free wall of the open-chest rat left ventricle. After pentobarbital anesthesia the hearts were arrested with 5 mM cadmium chloride and 0.9% saline and fixed with formaldehyde solution. Serial sections (250 microns thick) were cut from endocardium to epicardium with a freezing microtome. Selected sections were sonified, mixed with a gelatin-water solution, and placed on a glass slide. There was a progressive increase in mean sarcomere lengths with increasing intraventricular pressures though the sarcomeres did not significantly exceed their optimum length. There was a distinct and statistically significant difference in the pattern of sarcomere lengths through the ventricular wall between our previous closed-chest study and the present open-chest study. In this open-chest animals, there was an almost linear pattern of increasing sarcomere lengths from endocardium to epicardium over the range of semiphysiologic diastolic intraventricular pressures (6, 12, and 24 cm H2O -- 0.59, 1.18, 2.35 kPa). These results appear to caution against extrapolations on ventricular function derived from open chest studies to the normal physiologic conditions.