Differentiating the role of extracellular matrix and intracellular structures of myocardium in the total mechanical response of passive muscles now takes attention of researchers due to recently investigated nonlinear features of giant intracellular protein titin. We assume here that the variety of spatial structures on a fascicule level can be represented by 2D‐model consisting of inclined, longitudinal and transversal elastic springs and damping elements. The titin block (consisting of N=10 times repeated rhombic structure) is inserted in the bulk of parallelogram‐shaped fascicule block. Now we can calculate steady state stress‐strain curve, hysteresis loop, and stress relaxation under step‐wise stretching in the model with or without titin block.It was found that intracellular structures are the main sources of non‐linearity of stress‐strain relation. We have superimposed stress‐strain relations obtained for papillary muscle in normal conditions and after application of NaOH which disrupted intracellular structures of the muscle (Fig. 1A). The experimental protocol we used is shown on Fig. 1B (normal conditions) and after treatment of NaOH solution (Fig. 1C).Studying the difference in normal case and after treating with NaOH, we can evaluate the partial contribution of intracellular structures into passive mechanics of papillary muscles.This work is supported by RFBR URALS Grant #04‐04‐961091.

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The slow force response (SFR) of a cardiac muscle to a sudden stretch is thought to be important in the regulatory adaptation of myocardial contraction. Autocrine-paracrine regulation pathways which involve angiotensin II are participating in this mechanism. On the other hand, renin-angiotensin-aldosterone system (RAS) is altered in hypertrophic or failing myocardium. We compared the effects of sudden stretch to SFR as well as to twitch and Ca2+ transient characteristics in rat myocardium with monocrotaline-induced heart failure with those in normal rat myocardium without and with inhibition of angiotensin II type-1 (AT1) receptors. Our findings indicate that the myocardium of rats with monocrotaline-induced right ventricular failure is deficient with activation of local RAS and therefore expresses blunted SFR, very similar to the depression of SFR observed in normal myocardium under inhibition of AT1 receptors. The "failing" myocardium does not further respond to the "putative" inhibition of AT1 receptors by losartan. In conclusion, SFR is related to autocrine-paracrine regulation of myocardial contraction in normal rat myocardium and that the involvement of RAS into stretch-induced modulation of contractility may be significantly altered in failing heart.

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