Muscle Sympathetic Action Potential Firing Patterns During Normotensive and Hypertensive Pregnancy: A Longitudinal Assessment.
Muscle Sympathetic Action Potential Firing Patterns During Normotensive and Hypertensive Pregnancy: A Longitudinal Assessment.
复制标题
正常血压和高血压妊娠期间的肌肉交感神经动作电位放电模式：纵向评估。
DOI：
10.1161/circulationaha.122.062192
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发表时间：
2023
期刊：
影响因子：
37.8
通讯作者：
Fu,Qi
中科院分区：
文献类型：
--
作者：
Badrov,MarkB;Yoo,Jeung-Ki;Hissen,SarahL;D'Souza,AndrewW;Nelson,DavidB;Shoemaker,JKevin;Fu,Qi
妊娠期高血压（GH）是全球母婴发病率和死亡率的主要原因。其发病机制尚未完全阐明，但越来越多的证据表明，交感神经失调可能发挥重要作用。1，2在横截面设计中，我们最近证明，在妊娠晚期，与正常妊娠的女性相比，发生GH的女性显示出交感神经动作电位（AP）放电/综合爆发以及总AP放电频率的显著增加。3目前尚不清楚是否异常AP放电也存在于怀孕早期的妇女谁随后发展GH，当增加的肌肉交感神经活动（MSNA）爆发频率已经明显，1以及如何放电模式影响静息血压（BP）在整个妊娠期。因此，我们前瞻性地研究了整个正常血压和高血压妊娠期间静息多单位肌肉交感神经AP放电的模式。24名计划怀孕或在怀孕前8周内的健康非吸烟者在提供知情同意书后参加了研究。在妊娠前（黄体中期; n= 12）、妊娠早期（妊娠4 - 8周; n= 24）和妊娠晚期（妊娠32 - 36周; n= 24）以及产后（分娩后6 - 10周; n= 22）对女性进行纵向测试。分娩后，将女性分为2组：健康正常妊娠组（NP; n= 18;早期妊娠：31±5岁，70±12 kg;晚期妊娠：81±12 kg）和晚期妊娠试验后发生GH的患者（n= 6;早期妊娠：30±4岁，81±22 kg;晚期妊娠：93±19 kg），经临床诊断，如前所述。1、3无先兆子痫。该研究已获得机构审查委员会批准（STU-012011-198）。这些数据的一部分已被报告，以解决单独的，独特的假设。1，3在仰卧位休息期间，收集6分钟的心率、BP（血压电测法）和MSNA（显微神经描记法）。静息MSNA分析传统的测量，集成的神经图，并从我们的新方法来提取AP从过滤的原始MSNA信号，使用基于小波的方法。3多单位AP放电模式被量化为每个积分爆发的平均AP含量（尖峰/爆发）和AP频率（尖峰/分钟）。NP组的静息平均血压在整个妊娠期间均无变化（均P> 0.05）; GH组的静息平均血压从妊娠早期到晚期升高（P< 0.05），因此在妊娠晚期和产后高于NP组（均P< 0.05;图A）。妊娠晚期，NP和GH组的静息心率增加（与妊娠前相比均P< 0.05），但在整个妊娠期间，各组之间无差异（均P> 0.05;图，B）。NP和GH组的MSNA爆发频率在妊娠晚期增加（与妊娠前相比均P< 0.05）;正如预期，在妊娠早期和晚期以及产后，GH组的MSNA爆发频率更高（均P< 0.05;图C）。在妊娠前期，各组间平均AP含量相似（P> 0.05）;在妊娠晚期，
Gestational hypertension (GH) represents a leading cause of maternal–fetal morbidity and mortality worldwide. Its pathogenesis remains to be fully elucidated, but accumulating evidence suggests that sympathetic neural dysregulation may play an important role. 1, 2 In a cross-sectional design, we recently demonstrated that during late pregnancy, women who develop GH display a marked augmentation of sympathetic action potential (AP) firing per integrated burst, as well as total AP firing frequency, compared with women with normal pregnancies. 3 It remains unknown whether aberrant AP discharge also is present during early pregnancy in women who subsequently develop GH, when increased muscle sympathetic nerve activity (MSNA) burst frequency is already manifest, 1 and how such firing patterns influence resting blood pressure (BP) throughout gestation. Therefore, we investigated prospectively the patterning of resting multiunit muscle sympathetic AP discharge throughout both normotensive and hypertensive pregnancies. Twenty-four otherwise healthy nonsmokers who were planning to become pregnant or were within the first 8 weeks of pregnancy participated after providing informed consent. Women were tested longitudinally before pregnancy (midluteal phase; n= 12), during early (4 to 8 weeks of gestation; n= 24) and late pregnancy (32 to 36 weeks of gestation; n= 24), and postpartum (6 to 10 weeks after delivery; n= 22). After delivery, women were divided into 2 groups: those with healthy, normal pregnancies (NP; n= 18; early pregnancy: 31±5 years, 70±12 kg; late pregnancy: 81±12 kg) and those who developed GH after their late pregnancy testing (n= 6; early pregnancy: 30±4 years, 81±22 kg; late pregnancy: 93±19 kg), diagnosed clinically, as detailed previously. 1, 3 None developed preeclampsia. The study received institutional review board approval (STU-012011-198). Parts of these data have been reported to address separate, unique hypotheses. 1, 3 Heart rate, BP (electrosphygmomanometry), and MSNA (microneurography) were collected for 6 minutes during supine rest. Resting MSNA was analyzed from the traditionally measured, integrated neurogram and from our novel approach to extract APs from the filtered raw MSNA signal, using wavelet-based methodology. 3 Multiunit AP firing patterns were quantified as the mean AP content per integrated burst (spikes/burst) and AP frequency (spikes/min). Resting mean BP was unchanged throughout gestation in NP (all P> 0.05); in GH, it increased from early to late pregnancy (P< 0.05) and thus was greater than NP during late pregnancy and postpartum (both P< 0.05; Figure, A). Resting heart rate increased during late pregnancy in NP and GH (both P< 0.05 versus prepregnancy), but no differences existed between groups throughout gestation (all P> 0.05; Figure, B). MSNA burst frequency increased during late pregnancy in NP and GH (both P< 0.05 versus prepregnancy); as anticipated, 1 throughout early and late pregnancy, and postpartum, it was greater in GH (all P< 0.05; Figure, C). During prepregnancy, the mean AP content per burst was similar between groups (P> 0.05); it increased during late