Crampin Edmund J, Smith Nicolas P, Langham A Elise, Clayton Richard H, Orchard Clive H
Bioengineering Institute, The University of Auckland, Private Bag 92019 Auckland, New Zealand.
Philos Trans A Math Phys Eng Sci. 2006 May 15;364(1842):1171-86. doi: 10.1098/rsta.2006.1763.
The effects of acidosis on cardiac electrophysiology and excitation-contraction coupling have been studied extensively. Acidosis decreases the strength of contraction and leads to altered calcium transients as a net result of complex interactions between protons and a variety of intracellular processes. The relative contributions of each of the changes under acidosis are difficult to establish experimentally, however, and significant uncertainties remain about the key mechanisms of impaired cardiac function. In this paper, we review the experimental findings concerning the effects of acidosis on the action potential and calcium handling in the cardiac ventricular myocyte, and we present a modelling study that establishes the contribution of the different effects to altered Ca2+ transients during acidosis. These interactions are incorporated into a dynamical model of pH regulation in the myocyte to simulate respiratory acidosis in the heart.
酸中毒对心脏电生理学和兴奋-收缩偶联的影响已得到广泛研究。酸中毒会降低收缩强度,并由于质子与多种细胞内过程之间的复杂相互作用,最终导致钙瞬变改变。然而,酸中毒时每种变化的相对贡献很难通过实验确定,心脏功能受损的关键机制仍存在重大不确定性。在本文中,我们回顾了有关酸中毒对心室肌细胞动作电位和钙处理影响的实验结果,并提出了一项建模研究,该研究确定了酸中毒期间不同效应对Ca2+瞬变改变的贡献。这些相互作用被纳入心肌细胞pH调节的动力学模型中,以模拟心脏的呼吸性酸中毒。