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Figure 1 | BioMedical Engineering OnLine

Figure 1

From: Ischemia reperfusion dysfunction changes model-estimated kinetics of myofilament interaction due to inotropic drugs in isolated hearts

Figure 1

Block diagram of a biochemical model relating the input/output relationship between myoplasmic [Ca2+] and LVP adapted from Baran et al.[7] and Shimizu et al.[8] The 4-state model is governed by 5 differential equations. TnCA represents the troponin C molecule on the actin (A) myofilament, M represents the myosin head, + indicates weak bonds and • represents strong bonds. The sequence of events from phasic [Ca2+] to contraction are as follows: Ca2+ binds to TnCA, tropomyosin shifts so M and A can bind forming an actinomyosin cross-bridge, Ca2+ dissociates from TnCA with cross-bridge attached, and finally the cross-bridge breaks. Model rate constants and their units are indicated by their sites of action and described in Table 1. Note that A and M cannot form cross-bridges in the absence of Ca2+; however, since this is a loose coupling model, once a cross-bridge has been formed it no longer requires associated Ca2+ to remain attached.

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