Contractile dysfunction of cardiomyopathic hamster myocytes is pronounced under high load conditions

Phosphorylation Status of Regulatory Proteins and Functional Characteristics in Myocardium of Dilated Cardiomyopathy of Syrian Hamsters

“…In our earlier study [7], the calcium transients measured by Indo-1 was found to reveal elevated diastolic levels, decreased peak levels, and slower diastolic decay in TO-2 myocytes as compared with F1B myocytes. From these results together with the previous similar findings [12,13], the contractile dysfunctions in TO-2 heart have been considered to be caused mostly by the impairment of the sarcoplasmic reticulum calcium transport function.…”

“…Bio TO-2 strain hamster with congenital DCM shows similar clinical backgrounds to human cases and thus has been considered to be a representative animal model of human hereditary dilated cardiomyopathy [2][3][4][5][6][7]. The gene defect in δ-sarcoglycan has been identified as being responsible for DCM in TO-2 hamster [8,9] as well as in human [10].…”

“…The subcellular mechanism accounting for the myocyte dysfunction, however, remains to be characterized, though it is reported to very likely include the abnormalities of the sarcolemma, the sarcoplasmic reticulum, and the myofibrils [11][12][13]. Recently, we [7] studied the contractile function of myocytes isolated from the ventricles of 10-to 12-week-old TO-2 hamsters over a wide range of loading conditions and found that (1) in the unloaded condition, the shortening fraction and maximum shortening velocity were decreased in TO-2 myocytes as compared with normal control (F1B strain hamster) myocytes; (2) the peak force in the isometric condition and the external work in physiologically loaded conditions were also decreased. Being consistent with these contractile dysfunctions, the calcium transients measured by Indo-1 were found to reveal an elevated diastolic level, a decreased peak level, and a slower diastolic decay in TO-2 myocytes as compared with F1B myocytes.…”

Design, fabrication, and testing of a microfluidic system for cardiac cell culture.

“…[23] When the muscle is stretched to a length greater than normal size, new sarcomere units are added rapidly at the end of the muscle fibers. [22,24] Unlike the skeletal muscle, sarcomere length in cardiac muscle does not change very much, and small change in sarcomere length can result large changes in tension generation. [23 , 25-26] Therefore, increasing the sarcomere length enhances the tension development, which affects the changes both in preload condition and the contractility of the heart.…”

“…The remodeling of the hearts causes to increase the number of fibroblasts, thickens the heart muscle wall, or enlargers the size of the hearts. [24,[27][28] …”