Search for author "Zhilin Qu"

A, Interconnectedness of K⁺, Na⁺, and Ca²⁺ balances in the cardiac myocyte. Outward K⁺ loss through K⁺ channels (left) is recovered by the Na⁺-K⁺ ATPase removing 3 Na⁺ ions in exchange for 2 K⁺ ions. Some Na⁺ ions enter the cell via Na⁺ channels, but most via Na⁺-Ca²⁺ exchange (NCX) during diastole, which exchanges 1 Ca²⁺ ion for 3 Na⁺ ions. In the steady state, the Ca²⁺ removed by NCX balances the Ca²⁺ entering the cell via Ca²⁺ channels. Most Ca²⁺ in the cell recycles between the sarcoplasmic reticulum (SR) and cytoplasm, with uptake by sarcoendoplasmic reticulum Ca²⁺ ATPase (SERCA) and release through ryanodine receptors (RyR). Cytoplasmic free Ca²⁺ activates Ca²⁺-calmodulin kinase (CaMK), which regulates the properties of Na⁺, Ca²⁺, and K⁺ channels, and RyR in the SR (dotted arrows). B, Effects of hypokalemia on the action potential (AP). Superimposed AP recordings from an isolated rabbit ventricular myocyte with [K⁺]_o=5.4 mmol/L (black trace) vs [K⁺]_o=2.7 mmol/L (red trace), showing hyperpolarized E_m and early afterdepolarizations (EADs), the latter suppressed by the CaMK blocker KN-93 (green trace), but not by inactive KN-92 (blue trace). Adapted from Pezhouman et al¹ with permission of the publisher. Copyright © 2015, American Heart Association. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

Regional chaos synchronization of early afterdepolarizations (EADs) in tissue. In simulated paced homogeneous cardiac tissue, electrotonic coupling causes regional chaos synchronization to generate EAD islands (red regions), separated by regions without EADs (blue), whose position and size vary from beat to beat. Beat No. 1 illustrates a scenario in which a triggered premature ventricular contraction (★) arising from an EAD island blocks superiorly (dashed line) but conducts inferiorly (solid line), subsequently reentering the blocked region to induce reentry. Beat No. 2 illustrates a scenario in which the triggered premature ventricular contraction arising from an EAD island encounters another EAD island, resulting in conduction block (dashed line) and reentry (solid lines). Adapted from Weiss et al⁶ with permission of the publisher. Copyright © 2015, Elsevier. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

Phase 2 reentry during simulated ischemia in canine epicardium. Traces show action potential (AP) recordings from 4 sites (Epi 1–4) in a canine epicardial sheet exposed to simulated ischemia ([K⁺]_o=6 mmol/L, hypoxia, pH=6.8). Sites 1 and 2 exhibit normal APs with accentuated AP domes, whereas sites 3 and 4 show early repolarization. Arrows show reexcitation of site 3 by the AP dome at site 2, inducing phase 2 reentry that self-terminates after 4 beats. Adapted from Lukas and Antzelevitch⁴² with permission of the publisher. Copyright © 1996, Oxford University Press. Authorization for this adaptation has been obtained both from the owner of the copyright in the original work and from the owner of copyright in the translation or adaptation.

Ventricular arrhythmias after injection of KCl (2.8 mg/kg) into the left anterior descending coronary artery of a dog at the times indicated in A–E. Reprinted from Harris et al⁵⁰ with permission of the publisher. Copyright © 1954, the American Association for the Advancement of Science.