近期有子痫前期病史的妇女对手握运动的血压反应会增强,但对呼吸暂停或精神压力的反应不会增强

Danielle E. Berbrier, Tessa E. Adler, Cheryl A. Leone, Michael J. Paidas, Nina S. Stachenfeld, Charlotte W. Usselman
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引用次数: 0

摘要

先兆子痫是未来心血管疾病的一个风险因素。然而,这种关联的机制仍不清楚,从而限制了有效的预防策略。血压对急性刺激的反应可揭示静息状态下不明显的心血管功能障碍,从而识别心血管风险升高的个体。因此,我们比较了曾患有先兆子痫(PPE)的妇女(34±5 岁,产后 13±6 个月)和健康妊娠妇女(CTRL;29±3 岁,产后 15±4 个月)对急性刺激的血压反应。在呼气末呼吸暂停、精神紧张和等长手握运动方案期间,对血压(根据手动血压计得出的值校准的手指血压计;PPE:12 人,CTRL:12 人)进行了评估。对一部分参与者的综合肌肉交感神经活动(MSNA)进行了评估(腓肠神经微神经电图;PPE:n=6,CTRL:n=8)。在所有方案中,PPE 的收缩压 (SBP) 均高于 CTRL(组别的主效应均为 P<0.05)。SBP 的峰值变化具有应激特异性:在呼吸暂停(+8±6 vs. +6±5mmHg,P=0.32)或精神压力(+9±5 vs. +4±7mmHg,P=0.06)时,PPE 和 CTRL 的 SBP 峰值增加没有差异。然而,PPE 运动引起的 SBP 峰值升高比 CTRL 更大(+11±5 vs. +7±7mmHg,P=0.04)。在所有方案中,PPE 的 MSNA 均高于 CTRL(各组的主效应均为 P<0.05),在呼吸暂停(+44±6 vs. +27±14burst/100hb, P=0.04)和运动(+25±8 vs. +13±11burst/100hb, P=0.01)时,PPE 的 MSNA 峰值增加高于 CTRL,但在精神压力时,各组间无差异(+2±3 vs. 0±5burst/100hb, P=0.41)。对某些刺激的过度加压和交感反应可能是 PPE 长期罹患心血管疾病风险升高的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blood pressure responses to handgrip exercise but not apnea or mental stress are enhanced in women with a recent history of preeclampsia
Preeclampsia is a risk factor for future cardiovascular diseases. However, the mechanisms underlying this association remain unclear, limiting effective prevention strategies. Blood pressure responses to acute stimuli may reveal cardiovascular dysfunction not apparent at rest, identifying individuals at elevated cardiovascular risk. Therefore, we compared blood pressure responsiveness to acute stimuli between previously preeclamptic (PPE) women (34±5yr, 13±6 months postpartum) and women following healthy pregnancies (CTRL; 29±3yr, 15±4 months postpartum). Blood pressure (finger photoplethysmography calibrated to manual sphygmomanometry-derived values; PPE: n=12, CTRL: n=12) was assessed during end-expiratory apnea, mental stress, and isometric handgrip exercise protocols. Integrated muscle sympathetic nerve activity (MSNA) was assessed in a subset of participants (peroneal nerve microneurography; PPE: n=6, CTRL: n=8). Across all protocols, systolic blood pressure (SBP) was higher in PPE than CTRL (main effects of group all P<0.05). Peak changes in SBP were stressor-specific: peak increases in SBP were not different between PPE and CTRL during apnea (+8±6 vs. +6±5mmHg, P=0.32) or mental stress (+9±5 vs. +4±7mmHg, P=0.06). However, peak exercise-induced increases in SBP were greater in PPE than CTRL (+11±5 vs. +7±7mmHg, P=0.04). MSNA was higher in PPE than CTRL across all protocols (main effects of group all P<0.05), and increases in peak MSNA were greater in PPE than CTRL during apnea (+44±6 vs. +27±14burst/100hb, P=0.04) and exercise (+25±8 vs. +13±11burst/100hb, P=0.01) but not different between groups during mental stress (+2±3 vs. 0±5burst/100hb, P=0.41). Exaggerated pressor and sympathetic responses to certain stimuli may contribute to the elevated long-term risk for cardiovascular disease in PPE.
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