Mechanical properties of isolated cardiac myocytes

A wide variety of techniques have been developed to monitor the mechanical responses of isolated cardiac myocytes. The most successful are those that measure shortening in unattached cells. Because of their relative ease of implementation, edge-detector methods of following cell displacement have become most widespread. Laser diffraction techniques have been applied to the single heart cells, and sophisticated sarcomere imaging systems capable of 2-ms time resolution of shortening responses have also been developed. Active force has been recorded in intact single cells from frog atria; however, the compliance of the force transducers was relatively higher (approximately 5% Lo). (There is an obvious trade-off between transducer sensitivity, which affects noise and drift and compliance.) Some success has been reported with the use of intact rat myocytes supported by suction micropipettes and in guinea pig ventricular myocytes adhering to poly-L-lysine-coated glass beams. With the rat preparation, contractile stress was comparable to that of ventricular muscle, but few cells survived the attachment. In guinea pig myocytes, contractile stress in electrically induced twitches was only approximately 10% of the active stress developed by mammalian trabeculae or papillary muscles at the same temperature (35 degrees C), but, as with the frog atrial transducer, the compliance of the supporting beams was relatively high. Sarcomere uniformity has not been evaluated in these intact preparations. For attachment to the relatively short mammalian cardiac myocytes, the more promising methods that better preserve sarcomere uniformity include double-barreled micropipettes coated with a barnacle adhesive; however, for nonsubmersible transducers, a continuing limitation is the problem of solution surface stability. Unfortunately, the more severe limitation to effective attachment to intact cells is still the extreme sensitivity of the sarcolemma to mechanical stress. The challenge remains to develop an attachment to the intercalated disk such that cell stress can be transferred to the supporting transducers along the normal stress-bearing cellular interface. The ultrastructural and passive mechanical data strongly indicate that although the extracellular collagen limits the extension of cardiac muscle beyond the peak of the active length-tension relation, there is also a substantial cellular component of resistance to extension. Furthermore, this cellular component is related to the cytoskeleton rather than to membranous elements in the cell. The more likely candidates for the longitudinal resting stress-bearing element are titin (connectin) and desmin.(ABSTRACT TRUNCATED AT 400 WORDS)