Mikane, Suga, Araki, Kohno, Nakayama, Suzuki, Shimuzi, Matsubara, Hirakawa, Takaki, 1997

Model Status

This model is known to run in both OpenCell and COR. It is an accurate match to the paper equations but it does not recreate all the published results.

Model Structure

Abstract: We have reported that, in canine hearts, cardiac cooling to 29C enhanced left ventricular contractility but changed neither the contractile efficiency of cross-bridge (CB) cycling nor the excitation-contraction coupling energy. The mechanism of this intriguing energetics remained unknown. To get insights into this mechanism, we simulated myocardial cooling mechanoenergetics using basic Ca2+ and CB kinetics. We assumed that both adenosinetriphosphatase (ATPase)-dependent sarcoplasmic reticulum (SR) Ca2+ uptake and CB detachment decelerated with cooling. We also assumed that all the ATPase-independent SR Ca2+ release, Ca2+ binding to and dissociation from troponin, and CB attachment remained unchanged. The simulated cooling shifted the CB force-free Ca2+ concentration curve to a lower Ca2+ concentration, increasing the Ca2+ responsiveness of CB force generation, and increased the maximum Ca2+-activated force. The simulation most importantly showed that these cooling effects combined led to a constant contractile efficiency when Ca2+ uptake and CB detachment rate constants changed appropriately. This result seems to account for our experimentally observed constant contractile efficiency under cooling inotropy.

Schematic diagram of the Mikane et al model. The effect of calcium and troponin on cross bridge (CB) cycling is also demonstrated.

The complete original paper reference is cited below:

Mechanism of constant contractile efficiency under cooling inotropy of myocardium: simulation, Takeshi Mikane, Junichi Araki, Kunihisa Kohno, Yasunori Nakayama, Shunsuke Suzuki, Juichiro Shimizu, Hiromi Matsubara, Masahisa Hirakawa, Miyako Takaki, and Hiroyuki Suga, 1997, American Journal of Physiology, 273, H2891-H2898. PubMed ID: 9435629

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