[ XXXX and changes in contractile function of cardiomyocyte].

@entity712 @entity82 @entity1283 @entity35 @entity11636
To investigate the cellular mechanisms of pressure-overload @entity1283 transition to @entity712 , we observed time course of changes in morphology and contractile function of cardiomyocytes in transverse abdominal aortic constriction (TAC) @entity35 . Since TAC @entity35 suffered higher stress, body weight had a slower growth rate compared with that of synchronous control @entity35 . Therefore, the left ventricular to body weight ratio produced experimental bias to evaluate the degree of @entity1283 . Length and width of collagenase-isolated cardiomyocyte were directly measured. Length, width and calculated surface area of cardiomyocyte showed a progressive increase in 8-, 16-, and 20-week TAC @entity35 . The increasing rate of surface area in cardiomyocytes was higher at the middle stage of TAC (from the eighth to sixteenth week). Due to the constraint of @entity82 formation, the increasing rate of surface area in cardiomyocytes was slower at the late stage of @entity11636 (from the sixteenth to twentieth week). The sarcomere length of cardiomyocytes was unchanged, whereas sarcomere numbers were significantly increased in 8-, 16-, and 20-week TAC @entity35 . Shortening amplitude of unloaded contraction in single cardiomyocyte was significantly enhanced in 1-week TAC @entity35 , but not altered in 8-week TAC @entity35 compared with that in the synchronous control @entity35 . On the contrary, unloaded shortening amplitude of single cardiomyocyte was significantly reduced in 16- and 20-week TAC @entity35 . The above results suggest that the reduced shortening amplitude may be associated with intrinsic molecular alterations in hypertrophied cardiomyocytes.
