Endothelial-Dependent Vasomotor Dysfunction in Infants After Cardiopulmonary Bypass.
Endothelial-Dependent Vasomotor Dysfunction in Infants After Cardiopulmonary Bypass.
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DOI：
10.1097/pcc.0000000000002049
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发表时间：
2020-01
期刊：
影响因子：
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通讯作者：
Lamb FS
中科院分区：
文献类型：
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作者：
Krispinsky LT;Stark RJ;Parra DA;Luan L;Bichell DP;Pietsch JB;Lamb FS
心脏搭桥术（CPB）诱导的内皮功能障碍已被推断为肺血管阻力的变化，循环生物标志物的改变，和术后毛细血管渗漏。在这种情况下，全身血管系统的内皮依赖性血管功能障碍从未被量化。本研究的目的是量化心肺转流对内皮血管控制的急性影响，并试图将这些影响与婴儿术后细胞因子、组织水肿和临床结局相关联。单中心前瞻性观察性队列试验研究。三级儿童医院儿科心脏ICU。1岁以下需要体外循环以修复先天性心脏病损的儿童。没有。激光多普勒灌注监测（LDPM）与乙酰胆碱（Ach，内皮依赖性血管扩张剂）或硝普钠（SNP，内皮非依赖性血管扩张剂）的局部离子导入相结合，以量化皮肤微循环中的内皮依赖性血管舒张功能。在术前、与CPB分离后2 - 4小时和24小时进行测量。15例患者完成了所有LPDM测量。比较分流前和分流后2 - 4小时的反应，Ach后峰值灌注（p = 0.0006）和剂量反应曲线下面积（p = 0.005）均降低，但对SNP的反应无变化。转流后24小时，对乙酰胆碱的反应性有所改善，但通常仍较基线低。术后前48小时内，内皮功能保持与较高的尿量相关（R2 = 0.43，p = 0.008）。皮肤内皮功能障碍存在于婴儿CPB后立即，并在一些患者术后24小时内显著恢复。证实持续性内皮依赖性血管功能障碍和尿量减少之间的关联可能具有重要的临床意义。正在进行的研究将探索CBP后内皮依赖性血管功能障碍的模式及其与炎症生化标志物和临床结局的关系。
Cardiopulmonary bypass (CPB)-induced endothelial dysfunction has been inferred by changes in pulmonary vascular resistance, alterations in circulating biomarkers, and post-operative capillary leak. Endothelial-dependent vasomotor dysfunction of the systemic vasculature has never been quantified in this setting. The objective of the current study was to quantify acute effects of cardiopulmonary bypass on endothelial vasomotor control and attempt to correlate these effects with post-operative cytokines, tissue edema, and clinical outcomes in infants. Single center prospective observational cohort pilot study. Pediatric Cardiac ICU at a tertiary children’s hospital. Children less than 1 year-old requiring cardiopulmonary bypass for repair of a congenital heart lesion. None. Laser Doppler perfusion monitoring (LDPM) was coupled with local iontophoresis of acetylcholine (Ach, endothelium-dependent vasodilator) or sodium nitroprusside (SNP, endothelium-independent vasodilator) to quantify endothelial-dependent vasomotor function in the cutaneous microcirculation. Measurements were obtained pre-operatively, 2–4 hours, and 24 hours after separation from CPB. Fifteen patients completed all LPDM measurements. Comparing pre-bypass with 2–4 hours post-bypass responses, there was a decrease in both peak perfusion (p=0.0006) and area under the dose response curve (p=0.005) following Ach, but no change in responses to SNP. Twenty-four hours after bypass responsiveness to Ach improved, but typically remained depressed from baseline. Conserved endothelial function was associated with higher urine output during the first 48 post-operative hours (R2=0.43, p=0.008). Cutaneous endothelial dysfunction is present in infants immediately following CPB and recovers significantly in some patients within 24 hours post-operatively. Confirmation of an association between persistent endothelial-dependent vasomotor dysfunction and decreased urine output could have important clinical implications. Ongoing research will explore the pattern of endothelial-dependent vasomotor dysfunction after CBP and its relationship with biochemical markers of inflammation and clinical outcomes.