窦房结膜钟和钙钟在缺血条件下对细胞自律性的调控

doi:10.3969/j.issn.0258-8021.2013. 04.05

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Abstract Ischemiainduced sinus bradycardia and beating pause are commonly occurred in clinics, but its ionic mechanisms are still not very clear. Based on the action potential dynamic model of the sinoatrial node cell (SANC), and by increasing the extracellular K⁺ and intracellular Na⁺ concentrations, enhancing Ltype Ca^2+ current I_CaL, decreasing NaCa exchange current I_NCX and Ttype Ca²⁺ current I_CaT, we simulated the ischemia and quantitatively studied the role of individual factor in SANC automaticity. Additionally, by developing a onedimensional SANatrium tissue model on the monodomain equation, the electrical propagation state and role of calcium clock were studied as well. Results showed that during ischemia the enhanced I_CaL and accumulation of K⁺had little impacts on automaticity. Although decreasing I_CaT by one time caused 13% drop in beating frequency, automaticity still remained. However, potential oscillation and even beating pause were found after elevating intracellular Na⁺by 10% or reducing I_NCX by 55%. Further study showed that the impact of intracellular Na⁺on automaticitywas actually realized through the indirect decrease of I_NCX.Therefore, we suggest that reduction of I_NCX is a crucial factor to cause sinus bradycardia and even pause during ischemia. In addition, during ischemia, the automaticity was able to recover through enhancing calcium clock activity, suggesting the synergistic membrane and calcium clocks are fundamentals to the automatic depolarization of SANC.

Key words： sinoatrial node membrane clock calcium clock ischemia action potential model

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	ZHANG Hong^1*YANG Lin²ZHAO Wei³ZHENG Xiao^1

Cite this article:

ZHANG Hong^1*YANG Lin²ZHAO Wei³ZHENG Xiao^1. Automaticity Control by Membrane and Calcium Clocks in Ischemic Sinoatrial Node[J]. journal1, 2013, 32(4): 411-417.

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http://cjbme.csbme.org/EN/10.3969/j.issn.0258-8021.2013. 04.05 OR http://cjbme.csbme.org/EN/Y2013/V32/I4/411

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