Vesoulis Zachary A, Hao Jessica, McPherson Christopher, El Ters Nathalie M, Mathur Amit M
Division of Newborn Medicine, Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; and
Division of Newborn Medicine, Edward Mallinckrodt Department of Pediatrics, Washington University School of Medicine, St. Louis, Missouri; and.
J Appl Physiol (1985). 2017 Jul 1;123(1):55-61. doi: 10.1152/japplphysiol.00205.2017. Epub 2017 Apr 20.
The underlying mechanism as to why some hypotensive preterm infants do not respond to inotropic medications remains unclear. For these infants, we hypothesize that impaired vasomotor function is a significant factor and is manifested through a decrease in low-frequency blood pressure variability across regulatory components of vascular tone. Infants born ≤28 wk estimated gestational age underwent prospective recording of mean arterial blood pressure for 72 h after birth. After error correction, root-mean-square spectral power was calculated for each valid 10-min data frame across each of four frequency bands (, 0.005-0.0095 Hz; , 0.0095-0.02 Hz; , 0.02-0.06 Hz; and , 0.06-0.16) corresponding to different components of vasomotion control. Forty infants (twenty-nine normotensive control and eleven inotrope-exposed) were included with a mean ± SD estimated gestational age of 25.2 ± 1.6 wk and birth weight 790 ± 211 g. 9.7/11.8 Million (82%) data points were error-free and used for analysis. Spectral power across all frequency bands increased with time, although the magnitude was 20% less in the inotrope-exposed infants. A statistically significant increase in spectral power in response to inotrope initiation was noted across all frequency bands. Infants with robust blood pressure response to inotropes had a greater increase compared with those who had limited or no blood pressure response. In this study, hypotensive infants who require inotropes have decreased low-frequency variability at baseline compared with normotensive infants, which increases after inotrope initiation. Low-frequency spectral power does not change for those with inotrope treatment failure, suggesting dysfunctional regulation of vascular tone as a potential mechanism of treatment failure. In this study, we examine patterns of low-frequency oscillations in blood pressure variability across regulatory components of vascular tone in normotensive and hypotensive infants exposed to inotropic medications. We found that hypotensive infants who require inotropes have decreased low-frequency variability at baseline, which increases after inotrope initiation. Low-frequency spectral power does not change for those with inotrope treatment failure, suggesting dysfunctional regulation of vascular tone as a potential mechanism of treatment failure.
为何一些低血压早产儿对强心药物无反应,其潜在机制尚不清楚。对于这些婴儿,我们推测血管舒缩功能受损是一个重要因素,表现为整个血管张力调节成分的低频血压变异性降低。对估计胎龄≤28周的婴儿出生后72小时进行平均动脉血压的前瞻性记录。经过误差校正后,计算四个频段(,0.005 - 0.0095Hz;,0.0095 - 0.02Hz;,0.02 - 0.06Hz;以及,0.06 - 0.16)中每个有效10分钟数据帧的均方根谱功率,这些频段对应血管运动控制的不同成分。纳入40名婴儿(29名血压正常的对照婴儿和11名接受过强心药物治疗的婴儿),平均胎龄±标准差为25.2±1.6周,出生体重790±211克。970万/1180万(82%)个数据点无误差并用于分析。所有频段的谱功率均随时间增加,尽管接受过强心药物治疗的婴儿增加幅度小20%。在所有频段均观察到对开始使用强心药物后谱功率有统计学显著增加。对强心药物有强烈血压反应的婴儿比那些血压反应有限或无反应的婴儿增加幅度更大。在本研究中,与血压正常的婴儿相比,需要使用强心药物的低血压婴儿在基线时低频变异性降低,使用强心药物后增加。对于强心药物治疗失败的婴儿,低频谱功率没有变化,提示血管张力调节功能失调是治疗失败的潜在机制。在本研究中,我们研究血压正常和低血压且接受过强心药物治疗的婴儿在血管张力调节成分中血压变异性的低频振荡模式。我们发现,需要使用强心药物的低血压婴儿在基线时低频变异性降低,使用强心药物后增加。对于强心药物治疗失败的婴儿,低频谱功率没有变化,提示血管张力调节功能失调是治疗失败的潜在机制。