选择性大脑岛皮质缺血性卒中后左心房微血管内皮功能障碍、心肌炎症和纤维化。
Left atrial microvascular endothelial dysfunction, myocardial inflammation and fibrosis after selective insular cortex ischemic stroke.
机构信息
Vulnerable Brain Laboratory, Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University. 339 Windermere Rd, London, ON N6A 5A5, Canada; Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada.
Heart & Brain Laboratory, Western University, 339 Windermere Rd, London, ON, N6G 5A5, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada; Department of Clinical Neurological Sciences, London Health Sciences Centre, Schulich School of Medicine and Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada; Department of Epidemiology & Biostatistics, Schulich School of Medicine & Dentistry, Western University, 339 Windermere Rd, London, ON N6A 5A5, Canada; Robarts Research Institute, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Lawson Research Institute, 750 Base Line Rd E, London, ON N6C 2R5, Canada.
出版信息
Int J Cardiol. 2019 Oct 1;292:148-155. doi: 10.1016/j.ijcard.2019.06.004. Epub 2019 Jun 2.
BACKGROUND
Insular cortex (IC) ischemic strokes are associated with increased risk of cardiac arrhythmias. We have previously hypothesized that the anatomical substrate for post-stroke neurogenic arrhythmias comprises stroke-induced left atrium (LA) coronary microvascular endothelial dysfunction (CMED), and myocardial inflammatory infiltration (MII) leading to myocardial fibrosis. We investigated whether selectively induced IC ischemic stroke in rats results in histopathological changes in the LA.
METHODS
Insular ischemic stroke was induced in 6-month old male Wistar rats via unilateral stereotaxic injection of endothelin-1 into the left or right IC. The control group consisted of rats injected with saline. We histologically examined the LA 28 days after stroke for CMED, MII, and fibrosis. We performed linear regression analyses to assess correlation between the 3 histopathological outcomes. We compared these findings in the distal LA and the LA-pulmonary vein border (LA-PV border), a region of rich autonomic innervation.
RESULTS
Right and left IC stroke led to CMED, MII, and fibrosis in the LA. MII was significantly correlated with CMED and fibrosis. The LA-PV border had significantly greater MII and fibrosis than the distal LA. There were no differences in coronary microvascular and myocardial changes between left and right IC strokes.
CONCLUSIONS
Left and right insular ischemic strokes resulted in CMED, MII, and fibrosis, the pathological hallmark of arrhythmogenic LA tissue. Since these changes were greater within the LA-PV border than in the distal LA tissue, the role of preganglionic fibers at the ganglionated plexi as part of neurogenic arrhythmogenesis warrants further investigation.
背景
岛叶皮层（IC）缺血性中风与心律失常风险增加有关。我们之前假设，中风后引起的神经源性心律失常的解剖学基础包括中风引起的左心房（LA）冠状微血管内皮功能障碍（CMED），以及导致心肌纤维化的心肌炎症浸润（MII）。我们研究了大鼠选择性诱导的 IC 缺血性中风是否会导致 LA 的组织病理学变化。
方法
通过向左侧或右侧 IC 立体定向注射内皮素-1，在 6 个月大的雄性 Wistar 大鼠中诱导岛叶缺血性中风。对照组由注射盐水的大鼠组成。我们在中风后 28 天对 LA 进行组织学检查，以评估 CMED、MII 和纤维化。我们进行线性回归分析以评估 3 种组织病理学结果之间的相关性。我们比较了 LA 远端和富含自主神经支配的 LA-肺静脉交界（LA-PV 交界）区域的这些发现。
结果
右侧和左侧 IC 中风导致 LA 中的 CMED、MII 和纤维化。MII 与 CMED 和纤维化显著相关。LA-PV 交界的 MII 和纤维化明显大于 LA 远端。左、右 IC 中风之间的冠状微血管和心肌变化没有差异。
结论
左、右岛叶缺血性中风导致 CMED、MII 和纤维化，这是心律失常性 LA 组织的病理标志。由于这些变化在 LA-PV 交界处比在 LA 远端组织中更大，因此神经源性心律失常发生中节前纤维在神经节丛中的作用值得进一步研究。
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