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心肌水肿的致心律失常潜能:间质渗透压诱导螺旋波和多个兴奋小波。

Arrhythmogenic Potential of Myocardial Edema: The Interstitial Osmolality Induces Spiral Waves and Multiple Excitation Wavelets.

作者信息

Kiseleva Diana G, Dzhabrailov Vitalii D, Aitova Aleria A, Turchaninova Elena A, Tsvelaya Valeriya A, Kazakova Maria A, Plyusnina Tatiana Yu, Markin Alexander M

机构信息

Laboratory of Cellular and Molecular Pathology of Cardiovascular System, Petrovsky National Research Centre of Surgery, 119991 Moscow, Russia.

Department of Biophysics, Faculty of Biology, Lomonosov Moscow State University, 119991 Moscow, Russia.

出版信息

Biomedicines. 2024 Aug 6;12(8):1770. doi: 10.3390/biomedicines12081770.

DOI:10.3390/biomedicines12081770
PMID:39200234
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11351629/
Abstract

Myocardial edema is a common symptom of pathological processes in the heart, causing aggravation of cardiovascular diseases and leading to irreversible myocardial remodeling. Patient-based studies show that myocardial edema is associated with arrhythmias. Currently, there are no studies that have examined how edema may influence changes in calcium dynamics in the functional syncytium. We performed optical mapping of calcium dynamics on a monolayer of neonatal rat cardiomyocytes with Fluo-4. The osmolality of the solutions was adjusted using the NaCl content. The initial Tyrode solution contained 140 mM NaCl (1T) and the hypoosmotic solutions contained 105 (0.75T) and 70 mM NaCl (0.5T). This study demonstrated a sharp decrease in the calcium wave propagation speed with a decrease in the solution osmolality. The successive decrease in osmolality also showed a transition from a normal wavefront to spiral wave and multiple wavelets of excitation with wave break. Our study demonstrated that, in a cellular model, hypoosmolality and, as a consequence, myocardial edema, could potentially lead to fatal ventricular arrhythmias, which to our knowledge has not been studied before. At 0.75T spiral waves appeared, whereas multiple wavelets of excitation occurred in 0.5T, which had not been recorded previously in a two-dimensional monolayer under conditions of cell edema without changes in the pacing protocol.

摘要

心肌水肿是心脏病理过程的常见症状,会导致心血管疾病加重并引发不可逆的心肌重塑。基于患者的研究表明,心肌水肿与心律失常有关。目前,尚无研究探讨水肿如何影响功能合胞体中钙动力学的变化。我们使用Fluo-4对新生大鼠心肌细胞单层进行了钙动力学光学映射。通过调整NaCl含量来调节溶液的渗透压。初始的台氏液含有140 mM NaCl(1T),低渗溶液含有105(0.75T)和70 mM NaCl(0.5T)。本研究表明,随着溶液渗透压降低,钙波传播速度急剧下降。渗透压的连续降低还显示出从正常波前向螺旋波以及伴有波破裂的多个激发小波的转变。我们的研究表明,在细胞模型中,低渗以及由此导致的心肌水肿可能会引发致命的室性心律失常,据我们所知,此前尚未对此进行过研究。在0.75T时出现螺旋波,而在0.5T时出现多个激发小波,这在二维单层细胞水肿且起搏方案不变的条件下此前未曾记录到。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/582e0ea4f155/biomedicines-12-01770-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/8603a3d8b9c2/biomedicines-12-01770-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/caacb6087de4/biomedicines-12-01770-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/48a8275a0ea5/biomedicines-12-01770-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/b04ade79c785/biomedicines-12-01770-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/582e0ea4f155/biomedicines-12-01770-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/8603a3d8b9c2/biomedicines-12-01770-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/caacb6087de4/biomedicines-12-01770-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/48a8275a0ea5/biomedicines-12-01770-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/b04ade79c785/biomedicines-12-01770-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4b1/11351629/582e0ea4f155/biomedicines-12-01770-g005.jpg

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