Impaired pulmonary blood flow distribution in congestive heart failure assessed using synchrotron radiation microangiography.
Impaired pulmonary blood flow distribution in congestive heart failure assessed using synchrotron radiation microangiography.
复制标题
使用同步辐射微血管造影评估充血性心力衰竭的肺血流分布受损。
DOI：
10.1107/s0909049513007413
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发表时间：
2013
影响因子：
2.5
通讯作者：
Umetani K. Schwenke DO.
中科院分区：
文献类型：
--
作者：
Shirai M;Beard M;Pearson JT;Son obe T;Tsuchimochi H;Fujii Y;Gray E;Umetani K. Schwenke DO.
同步辐射微血管造影是评估与原发性肺动脉高压（PH）相关的肺血管密度不良变化的有力工具。充血性心力衰竭 (CHF) 会导致“继发性”PH 发作，但尚不清楚继发性 PH 是否也与血管密度降低有关。本研究利用同步加速器辐射评估患有继发性 PH 的 CHF 的 Dahl 大鼠模型中的肺血管密度和内皮功能。高盐喂养的 Dahl 盐敏感 (Dahl-S) 和耐盐 (Dahl-R) 大鼠被麻醉，并进行微血管造影，以评估肺血管密度和血管对 (i) 硝普钠 (5.0 μg kg−1 min−1)、(ii) 乙酰胆碱 (3.0 μg kg−1 min−1) 和 (iii) ET-1A 受体阻断的反应， BQ-123（1 mg kg−1）。 Dahl-S 大鼠出现 CHF 和继发性 PH，表现为内皮功能障碍、对乙酰胆碱的血管舒张反应受损、对 BQ-123 的血管舒张反应增强以及广泛的肺血管重塑。结果，肺血管密度不利地降低。有趣的是，继发性 PH 的病因表现为结构和功能的变化，与之前报道的原发性 PH 的变化相当。然而，一个重要的差异是，在继发性 PH 中，ET-1 对肺血管的调节在直径范围为 100-200μm 的血管中最为显着，而在原发性 PH 中，直径范围为 200-300μm 的血管则相反。在未来调查原发性和继发性 PH 的研究中应考虑此类差异。
Synchrotron radiation microangiography is a powerful tool for assessing adverse changes in pulmonary vessel density associated with primary pulmonary hypertension (PH). Congestive heart failure (CHF) leads to a `secondary' onset of PH, yet it is unknown whether secondary PH is also associated with reduced vessel density. This study utilized synchrotron radiation to assess both pulmonary vessel density and endothelial function in a Dahl rat model of CHF with secondary PH. High salt-fed Dahl salt-sensitive (Dahl-S) and salt-resistant (Dahl-R) rats were anesthetized and microangiography was performed to assess the pulmonary vessel density and vascular responses to (i) sodium nitroprusside (5.0 µg kg−1 min−1), (ii) acetylcholine (3.0 µg kg−1 min−1) and (iii) ET-1A receptor blockade, BQ-123 (1 mg kg−1). Dahl-S rats developed CHF and secondary PH as evident by endothelial dysfunction, impaired vasodilatory responses to acetylcholine, enhanced vasodilatory responses to BQ-123 and extensive pulmonary vascular remodeling. Consequently, the pulmonary vessel density was adversely reduced. Interestingly, the etiology of secondary PH manifests with structural and functional changes that are comparable with that previously reported for primary PH. One important discrepancy, however, is that ET-1 modulation of pulmonary vessels is most striking in vessels with a diameter range of 100–200 µm in secondary PH, in contrast to a range of 200–300 µm in primary PH. Such discrepancies should be considered in future studies investigating primary and secondary forms of PH.