Background: Cardiac remodeling underpinning progressive hypertensive heart disease alters the three-dimensional structure of the extracellular matrix, as well as the laminar organization of myocardial sheetlets. The effect of pharmacological intervention on microstructural remodeling is not known. Objective: To examine the changes in myocardial microstructure that occur as a result of hypertensive heart disease, and the effect of pharmacological treatment. Methods: The spontaneously hypertensive rat (SHR) model of hypertensive heart disease was studied, and compared with the normotensive Wistar Kyoto (WKY) rat, and SHRs treated with angiotensin converting enzyme inhibitors (TSHR). Cardiac magnetic resonance was used to assess cardiac function and ventricular geometry. Excised myocardium was stained (picrosirius red) for collagen and extended volume confocal microscopy used to produce high-resolution image stacks. Results: At 24 months, TSHRs had significantly greater ejection fraction ( P < 0.05 ), and performed significantly less stroke work than the untreated diseased SHRs ( P < 0.01 ). TSHR hearts displayed no increased collagen deposition between sheetlets at 14 months, unlike SHR hearts at the same age, which showed thick collagen and scarring. Laminar organization was retained in aged TSHR hearts, while it was progressively lost in aged SHR hearts. Conclusions: In aged SHRs, angiotensin converting enzyme inhibition attenuates remodeling of myocardial extracellular matrix, preserves the laminar organization of myocardial sheetlets, and helps to maintain normal cardiac function.

中文翻译：

---

心肌层状组织保留在血管紧张素转化酶抑制剂处理的 SHR 中

背景：支持进行性高血压心脏病的心脏重塑改变了细胞外基质的三维结构，以及心肌小片的层状组织。药物干预对微观结构重塑的影响尚不清楚。目的：探讨高血压性心脏病引起的心肌微结构变化及药物治疗的效果。方法：对自发性高血压大鼠（SHR）高血压心脏病模型进行研究，并与血压正常的Wistar京都（WKY）大鼠和血管紧张素转换酶抑制剂（TSHR）治疗的SHRs进行比较。心脏磁共振用于评估心脏功能和心室几何形状。切除的心肌被染色（天狼星红）以获得胶原蛋白和用于产生高分辨率图像堆栈的扩展体积共聚焦显微镜。结果：在 24 个月时，TSHRs 的射血分数显着更高（ P < 0.05 ），并且比未治疗的患病 SHRs 执行的卒中工作显着减少（ P < 0.01 ）。TSHR 心脏在 14 个月时没有显示出小片之间的胶原沉积增加，这与同龄的 SHR 心脏不同，后者显示出较厚的胶原蛋白和疤痕。层流组织在老化的 TSHR 心脏中保留，而在老化的 SHR 心脏中逐渐丢失。结论：在老年SHRs中，血管紧张素转化酶抑制作用减弱了心肌细胞外基质的重构，保护了心肌小片的层状组织，有助于维持正常的心功能。