To investigate how cardiomyocytes change their length, echocardiographic and morphological studies were performed on rabbit hearts that were subjected to volume overload, overload removal, and repeated cycles of overload and overload removal. These conditions were created by arterio-venous fistula between the carotid artery and jugular vein, closure of the fistula, and cycles of repeatedly forming and closing fistula, respectively. After overload, hearts dilated and myocytes elongated. Intercalated disks repeatedly broadened and narrowed with a 2-day cycle, which continued for 8 weeks in many animals. The cycle consisted of shifts between five modes characterized by two interdigitation elongation-and-shortenings as follows: (I) flat with short (ϳ1/4 to ϳ1/3 sarcomere long) interdigitations; (II) flat with long (one sarcomere long) interdigitations; (III) grooved with short interdigitations; (IV) grooved with long interdigitations; (V) flat with short interdigitations intermingled by sporadic long interdigitations; and return to (I). After overload removal, hearts contracted and myocytes shortened with similar 2-day broadening and narrowing cycle of intercalated disks, in which the five modes were reversed. Repeated overload and overload removal resulted in the repetition of myocyte elongation and shortening. We hypothesize that a single elongation-and-shortening event creates or disposes one sarcomere layer, and the two consecutive elongation-and-shortenings occur complementarily to each other so that the disks return to their original state after each cycle. Our hypothesis predicts that intercalated disks weave and unravel one sarcomere per myocyte per day. (Am J

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To investigate the effects of volume loading of the heart, the endocardium was studied histologically and ultrastructurally. Thirteen adult female beagle dogs were used. An arterio-venous shunt was constructed between the right common carotid artery and the right external jugular vein in nine animals to induce a volume load. Four animals were used as controls. All were kept for 6-12 months. Heart weight, relative heart weight (heart weight/body weight), cardiac output index, stroke volume index and volumes of both ventricles in the experimental animals were significantly larger than in the controls. Shunted blood volume was significantly correlated with heart weight. The endocardium of the left ventricle in the experimental animals showed elastofibrosis and was significantly thicker than in the controls. In 5 hearts, it was more than 2 0 p m thick and its endothelial cells showed many long microvilli with a very thick basement membrane (1.5-2.0pm).The thickness of the endocardium was significantly correlated with the heart weight, relative heart weight and cardiac output index, within 1% 5% and 5% risk, respectively. These endocardial changes were thought to be induced by hemodynamic changes in the left ventricle of the volume-loaded heart, probably being correlated with changes in cardiac function and morphology. Acta Pathol Jpn 39: 111-120, 1989.

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