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{"title":"Carotid Baroreceptor Magnetic Activation and Beat-to-Beat Blood Pressure Variability, Implications to Treat Abrupt Blood Pressure Elevation in Labile Hypertension","authors":"Juraj Gmitrov","doi":"10.1002/bem.22425","DOIUrl":null,"url":null,"abstract":"<p>Mounting evidence suggests enhanced blood pressure (BP) variability (BPV) independent role in cardiovascular (CV) damage. The goal was to estimate the effect of the carotid baroreceptor (CB) magnetic stimulation on sudden high BP elevation. Mean femoral arterial BP (MAP), heart rate (HR), baroreflex sensitivity (BRS), and ear lobe skin microcirculatory blood flow, by microphotoelectric plethysmography (MPPG), were simultaneously recorded in conscious rabbits sedated by pentobarbital intravenous (i.v.) infusion (5 mg/kg/h) after 40 min CB exposure to 350 mT static magnetic field (SMF), by Nd<sub>2</sub>-Fe<sub>14</sub>-B magnets (<i>n</i> = 14), or sham magnets exposure (<i>n</i> = 14). BRS was assessed from HR and MAP responses to abrupt hypotension induced by i.v. bolus injections of nitroprusside (Ni) and abrupt MAP elevation (MAP<sub>AE</sub>) by i.v. bolus of phenylephrine (Ph). Beat-to-beat BPV was estimated by MAP standard deviation. SMF CB exposure significantly increased BRS<sub>Ni</sub> (74.5 ± 17.8%, <i>P</i> < 0.001) and microcirculation (23.8% ± 11.0%, <i>P</i> = 0.039); decreased MAP (−5.7 ± 1.7%, <i>P</i> < 0.014) and phenylephrine-induced MAP<sub>AE</sub> (−19.1%, <i>P</i> = 0.043). MAP<sub>AE</sub> positively correlated with resting MAP (<i>r</i> = 0.342, <i>P</i> = 0.0383) and MAP SD (<i>r</i> = 0.383, <i>P</i> = 0.0194), and inversely with BRS<sub>Ph</sub> (<i>r</i> = −0.47, <i>P</i> = 0.0156). SMF CB exposure enhanced the nitroprusside, which acts by releasing nitric oxide (NO), vasodilatory effect. This indicates arterial baroreflex to improve vessel sensitivity to NO, which is a new physiology with BP buffering effect. A positive correlation of MAP SD to phenylephrine BP ramps suggests a causal relationship and BPV prognostic significance to forecast abrupt BP elevation. Mechano/baroreceptor magneto-sensing property proposed to be the basic physiology by which SMFs boost CV autonomic regulation with potential implementation in high CV risk labile arterial hypertensive disease. © 2022 Bioelectromagnetics Society.</p>","PeriodicalId":8956,"journal":{"name":"Bioelectromagnetics","volume":"43 7","pages":"413-425"},"PeriodicalIF":1.8000,"publicationDate":"2022-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bioelectromagnetics","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/bem.22425","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOLOGY","Score":null,"Total":0}
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Abstract
Mounting evidence suggests enhanced blood pressure (BP) variability (BPV) independent role in cardiovascular (CV) damage. The goal was to estimate the effect of the carotid baroreceptor (CB) magnetic stimulation on sudden high BP elevation. Mean femoral arterial BP (MAP), heart rate (HR), baroreflex sensitivity (BRS), and ear lobe skin microcirculatory blood flow, by microphotoelectric plethysmography (MPPG), were simultaneously recorded in conscious rabbits sedated by pentobarbital intravenous (i.v.) infusion (5 mg/kg/h) after 40 min CB exposure to 350 mT static magnetic field (SMF), by Nd2 -Fe14 -B magnets (n = 14), or sham magnets exposure (n = 14). BRS was assessed from HR and MAP responses to abrupt hypotension induced by i.v. bolus injections of nitroprusside (Ni) and abrupt MAP elevation (MAPAE ) by i.v. bolus of phenylephrine (Ph). Beat-to-beat BPV was estimated by MAP standard deviation. SMF CB exposure significantly increased BRSNi (74.5 ± 17.8%, P < 0.001) and microcirculation (23.8% ± 11.0%, P = 0.039); decreased MAP (−5.7 ± 1.7%, P < 0.014) and phenylephrine-induced MAPAE (−19.1%, P = 0.043). MAPAE positively correlated with resting MAP (r = 0.342, P = 0.0383) and MAP SD (r = 0.383, P = 0.0194), and inversely with BRSPh (r = −0.47, P = 0.0156). SMF CB exposure enhanced the nitroprusside, which acts by releasing nitric oxide (NO), vasodilatory effect. This indicates arterial baroreflex to improve vessel sensitivity to NO, which is a new physiology with BP buffering effect. A positive correlation of MAP SD to phenylephrine BP ramps suggests a causal relationship and BPV prognostic significance to forecast abrupt BP elevation. Mechano/baroreceptor magneto-sensing property proposed to be the basic physiology by which SMFs boost CV autonomic regulation with potential implementation in high CV risk labile arterial hypertensive disease. © 2022 Bioelectromagnetics Society.
颈动脉压力感受器磁激活和搏动血压变异性，对治疗不稳定高血压患者血压突然升高的影响
越来越多的证据表明，血压(BP)变异性(BPV)升高在心血管(CV)损伤中的独立作用。目的是评估颈动脉压力感受器(CB)磁刺激对突发性血压升高的影响。在350 mT静磁场(SMF)、Nd2-Fe14-B磁体(n = 14)或假磁体(n = 14)暴露40 min后，经戊巴比妥静脉注射(5mg /kg/h)镇静的清醒家兔，用微光电体积描记仪(MPPG)同时记录平均股动脉血压(MAP)、心率(HR)、气压反射敏感性(BRS)和耳垂皮肤微循环血流。通过静脉注射硝普苷(Ni)引起的突发性低血压和静脉注射苯肾上腺素(Ph)引起的突发性MAP升高(MAPAE)的HR和MAP反应来评估BRS。用MAP标准偏差估计搏动间BPV。SMF CB暴露显著增加BRSNi(74.5±17.8%，P < 0.001)和微循环(23.8%±11.0%，P = 0.039);降低MAP(- 5.7±1.7%，P < 0.014)和苯肾上腺素诱导的MAPAE (- 19.1%， P = 0.043)。MAPAE与静息MAP (r = 0.342, P = 0.0383)、MAP SD (r = 0.383, P = 0.0194)呈正相关，与BRSPh呈负相关(r = - 0.47, P = 0.0156)。SMF - CB暴露增强了硝普苷的血管舒张作用，硝普苷通过释放一氧化氮(NO)发挥作用。提示动脉压力反射提高血管对NO的敏感性，是一种具有BP缓冲作用的新生理机制。MAP SD与苯肾上腺素血压升高呈正相关，提示BP值与血压升高具有因果关系和预后意义。机械/压力感受器磁感特性被认为是smf促进心血管自主调节的基本生理机制，可能在心血管高危不稳定动脉高血压疾病中发挥作用。©2022生物电磁学学会。
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