迷走神经兴奋对HRV的影响及其机制的初步分析

实验在氯醛糖加氨基甲酸乙酯麻醉的新西兰兔上进行。记录血压、心率、心电图和心率变异性（ＨＲＶ）频谱分析。电刺激减压神经（ＤＮ）,疑核（ＮＡ）和右侧迷走神经（ＲＶ）外周端,均引起心率和血压下降（Ｐ＜０．００１）,总变异性（ＴＶ）、低频成分（ＬＦ）、高频成分（ＨＦ）、ＬＦ／ＨＦ比值（ＬＦ／ＨＦ）和极低频成分（ＶＬＦ）增大（Ｐ＜０．０５－０．００１）。静脉注射阿托品可使上述反应显著减小（Ｐ＜０．０５－０．０１）,而静脉注射心得安仅可阻断ＤＮ和ＮＡ所致ＬＦ的增大（Ｐ＜０．０５）。以上结果表明：迷走神经是ＨＲＶ的主要调节者之一;ＨＦ由迷走神经单独介导;ＬＦ受迷走神经和交感神经共同调制;迷走神经参与ＶＬＦ波的形成     

健康人不同年龄段HRV频谱分析及进食,心算的影响

应用上医大生理教研室研制的“心率变异性频谱分析仪”,以Ｒ－Ｒ间距总变异性（ＴＶ）、低频成分（ＬＦ）、高频成分（ＨＦ）以及ＬＰ／ＨＦ比值为指标,对健康人不同年龄段、午饭前后及安静与心算时的心率变异性（ＨＲＶ）进行频谱分析,结果表明：健康女性６０岁以上,男性５０岁以上各年龄段ＴＶ较低龄段显著降低,女性３０岁以上各年龄段及男性５０－６０岁ＬＦ、女性２０岁以上及男性２１－５０岁各年龄段ＨＦ均较低龄段升高显著,女性２１－３０岁较１－１０岁ＬＦ／ＨＦ降低显著;午饭后ＴＶ均较饭前显著降低,心算时ＬＦ显著升高,ＨＦ显著降低,≥４０岁组心算时ＬＦ／ＨＦ显著升高。结果提示：健康人高龄段调控心脏的自主神经整合功能显著降低,健康人的交感、迷走神经活动在不同年龄段有着不同的变化;健康成人午饭后自主神经整合功能显著降低;心算时交感神经活动显著增强,迷走神经活动显著降低,≥４０岁组心交感神经活动增强尤为显著。     

迷走神经和交感神经系统不同活动状态对心率变异性的影响

实验在氯醛糖加氨基甲酸乙酯麻醉的新西兰兔上进行。记录血压、心率、心电图并对心电Ｒ－Ｒ间期（ＲＲＩ）作功率谱密度（ＰＳＤ）分析。以单调性电刺激和低频率的波动性电刺激分别刺激减压神经、疑核和右侧迷走神经外周端,观察到低频率的波动性刺激对增加ＰＳＤ中低频成分（ＬＦ）的作用比单调性电刺激更大（Ｐ〈０．０５）。注射新福林仅在头一个２５６个心动周期时间内引起总变异性（ＴＶ）、ＬＦ、ＰＳＤ中高频成分（ＨＦ）。Ｌ     

蝮蛇抗栓酶伍用刺五加对冠心病心率变异性的影响

目的探讨蝮蛇抗栓酶伍用刺五加对冠心病心率异性的影响。方法观察蝮蛇抗栓酶伍用刺五加对冠心病变异性的影响,并与对照组对比。结果治疗组ＳＤＮＮ、ＨＦ、ＬＦ／ＨＦ改变较对照组有显著差异性（Ｐ＜０．０１）。结论该方法能显著提高冠心病患者的心率变异性,对冠心病心源性猝死的预防有着重要意义。     

NO对家兔Oddi括约肌肌电活动和血压的影响

应用３２只家兔观察一氧氮对Ｏｄｄｉ括约肌肌电和血压的影响。静脉注射ＮＯ合酶抑制剂Ｎ＾Ｇ－硝基－Ｌ－精氨酸,可见ＳＯ肌电振幅增大和血压升高,Ｌ－ＮＮＡ所致的肌电活动增强可Ｌ－精氨酸反转。     

延髓头端腹外侧区神经元电活动与心血管活动相干性的研究

本文分析了大鼠延头端腹外侧区（ＲＶＬＭ）神经元单位活动与心血管活动的相干性,观察了ＲＶＬＭ区神经元电 对电刺激中脑防御反应区的诱发反应,以及对压力感受性反射的反应,并用ＦＦＴ对ＲＶＬＭ区神经元自发单位放电和血压波进行频域的相干性分析,以判断是具有心节律。还分析了ＲＶＬＭ区单位放电变异性与心率变异性的相干性。结果显示：ＲＶＬＭ区大多数神经元对电刺激中脑防御反应区呈兴奋反应（６７％）,７０％神经元放电     

丽江产三尖杉的生物碱成分

丽江产三尖杉的生物碱成分邱明华陆保平＋马昕＋＋聂瑞麟（中国科学院昆明植物研究所,昆明６５０２０４）ＡＬＫＡＬＯＩＤＳＦＲＯＭＣＥＰＨＡＬＯＴＡＸＵＳＦＯＲＴＵＮＥＩＣＯＬＬＥＣＴＥＤＩＮＬＩＪＩＡＮＧＱｉｕＭｉｎｇｈｕａ,ＬｕＢａｏｐｉｎｇ＋,Ｍａ...     

臭灵丹中的黄酮醇成分

臭灵丹中的黄酮醇成分李顺林,丁靖垲（中国科学院昆明植物研究所植物化学开放研究室验室,昆明６５０２０４）关键词四棱峰属,臭灵丹,黄酮醇ＴＨＥＦＬＡＶＯＮＯＬＳＦＲＯＭＬＡＧＧＥＲＡＰＴＥＲＯＤＯＮＴＡ￥ＬＩＳｈｕｎ－Ｌｉｎ;ＤＩＮＧＪｉｎｇ－Ｋａｉ（Ｌ...     

蝮蛇抗栓酶伍用刺五加冠心病心率变异性的影响

目的 探讨蝮蛇抗栓酶伍用刺五加对冠心病心率异性的影响。方法 观察蝮蛇抗栓酶伍用刺五加对冠心病为异性的影响，并与对照组对比。结果 治疗组ＳＤＮＮ、ＨＦ、ＬＦ／ＨＦ改变较对照组有显著差异性（Ｐ〈０．０１）。结论 该方法能显著提高冠心病患者的心率变异性，对冠心病源性猝死的预防有着重要意义。     

FEN—1基因反义阻断细胞株（FL—FEN—1^—）的建立

ＦＥＮ－１是一咱结构特异性核酸酶,它在ＤＮＡ复制和修复过程中都起着重要的作用。将ＦＥＮ－１基因的ＮｃｏＩ－ＢａｍＨＩ片段反向克隆到哺乳动物细胞重组表达质粒ｐＭＡＭｎｅｏＡｍｐ＾－中,得到ＦＥＮ－１反义表达质粒ｐＭＡＭｎｅｏＡｍｐ＾－ＦＮＢ＾－,并转染ＦＬ细胞,经Ｇ４１８筛选后,获得ＦＥＮ－１基因表达被阻断的哺乳动物细胞ＦＬ－ＦＥＮ－１＾－。对细胞生长曲线的测定发现,ＦＬ－ＦＥＮ－１＾－在地塞米松的     

体位改变对Beagle犬心脏自主神经控制的影响

目的观察体位改变对Beagle犬心脏自主神经控制的影响。方法利用大动物无创生理遥测技术,监测清醒活动状态下雌性Beagle犬在静态姿势（lying、standing、sitting、hanging）和运动（walking）姿势下的心电图（ECG）,并用HRV功率谱分析其自主神经功能。结果在静态姿势下,Beagle犬RR间期（RRI）、RR间期的标准差SDNN（SDNN）、相邻RR间期差值平方和的均方根RMSSD（RMSSD）、相邻R-R间期差值〉50 ms的窦性个数占心搏总数的百分比pNNabs（50）（pNNabs（50））、TP总功率（TP）、VLF极低频功率（VLF）、标准化高频功率（HFnorm）均明显高于运动状态（P〈0.05,P〈0.01）,而心率（HR）、标准化低频功率（LFnorm）和低频功率/高频功率（LF/HF）平衡指数则明显低于运动状态（P〈0.05,P〈0.01）。结论不同体位姿势在静息状态下以迷走神经活动兴奋为主,相反,在运动状态下以交感神经活动兴奋为主;体位姿势改变能引起心率的变化,必然影响心脏自主神经控制能力,其主要取决于迷走神经活动强弱有关,且导致LF/HF均衡性的破坏。     

迷走神经在心率变异性中的作用

采用功率谱和近似熵 (approximateentropy ,ApEn)的方法 ,分析清醒家兔在双侧迷走神经保留 ,右、左侧迷走神经切断以及双侧迷走神经同时切断时心搏间期 (RRI)的变化。结果显示 :双侧迷走神经保留时功率谱中高频功率 (HF)、低频功率 (LF)及ApEn值均高于双侧及单侧迷走神经切断时 (P <0 0 5 ) ,LF/HF比值最小 ;切断单侧迷走神经 ,ApEn变小 ,LF/HF比值在右侧迷走神经切断时增大 ,而切断左侧迷走时LF/HF比值无明显变化 ;双侧迷走神经切断后LF/HF比值最大 ,ApEn最低。结果表明 :心率变异主要由迷走神经调节 ,右侧迷走神经起主要作用 ;传统心率变异性测量方法与非线性方法所得结果一致     

心房钠尿多肽对麻醉大鼠血压和肾神经传出放电的影响

本实验观察了心房肽Ⅱ(Atriopeptin Ⅱ,APⅡ)对麻醉大鼠血压(AP)、心率(HR)和肾交感神经传出放电(RSNA)的影响,并与硝普钠对 AP 和 RSNA 的影响作比较。结果如下:(1)缓冲神经完整和迷走神经完整条件下(n=12)静脉注射 APⅡ(50μg/kg)后,动脉收缩压(SAP)降低23.0±1.66 mmHg(Μ±SE,p<0.001),HR 减慢9±3.5b/min(p<0.05),RSNA 降低4.89±2.95%(P>0.05)。迷走神经切断后,静脉注射 APⅡ引起的~⊿SAP 虽有所减小,但与切断迷走神经前的反应比较,无统计学意义,HR 减慢不再出现,而 RSNA 则有所增加;(2)缓冲神经切断和迷走神经完整条件下(n=7),静脉注射 APⅡ时 SAP 降低27.4±3.25mmHg(P<0.001),HR 减慢13±3.1b/min(P<0.01),RSNA 降低11.67±1.95%(P<0.001)。切断迷走神经后,静脉注射 APⅡ引起的 SAP 降低程度有明显減小(P<0.01),HR减慢不再出现,RSNA 则反而增加(3)无论在迷走神经完整还是切断条件下,静脉注射硝普钠(n=6) SAP 均明显降低,同时伴有 RSNA 的反射性增加。以上结果表明:APⅡ的降压效应,部分是通过迷走神经传入纤维;在切断缓冲神经条件下,APⅡ可经由迷走神经传入纤维的激活而反射地抑制 RSNA。     

The nature of very low frequency component of the heart rate variability and the role of sympathetic-parasympathetic interactions

A method of separate monitoring "instant" changes of the VLF, LF and HF power spectral components of heart rate variability, has been developed. The power of the LF and HF spectral components were proved to be continuously changing. The period of these power fluctuations could stay within 15 to 150 sec. Comparison of the heart rate variability spectrum with LF and HF spectral components power fluctuations' spectrums has shown that the frequencies of the LF and HF spectral components power fluctuations stay within the VLF range. The co-operative spectrum form of these fluctuations repeats the form of the VLF peak. In cases when the LF and HF spectral components power fluctuations' periods do not coincide, VLF has two peaks. The frequency of one VLF peak coincides with frequency of the HF power fluctuations, and the frequency of another--with the frequency of LF power fluctuations.     

Respiratory-related heart rate variability in progressive experimental heart failure

Heart failure is associated with autonomic imbalance, and this can be evaluated by a spectral analysis of heart rate variability. However, the time course of low-frequency (LF) and high-frequency (HF) heart rate variability changes, and their functional correlates during progression of the disease are not exactly known. Progressive heart failure was induced in 16 beagle dogs over a 7-wk period by rapid ventricular pacing. Spectral analysis of heart rate variability and respiration, echocardiography, hemodynamic measurements, plasma atrial natriuretic factor, and norepinephrine was obtained at baseline and every week, 30 min after pacing interruption. Progressive heart failure increased heart rate (from 91 +/- 4 to 136 +/- 5 beats/min; P < 0.001) and decreased absolute and normalized (percentage of total power) HF variability from week 1 and 2, respectively (P < 0.01). Absolute LF variability did not change during the study until it disappeared in two dogs at week 7 (P < 0.05). Normalized LF variability increased in moderate heart failure (P < 0.01), leading to an increased LF-to-HF ratio (P < 0.05), but decreased in severe heart failure (P < 0.044; week 7 vs. week 5). Stepwise regression analysis revealed that among heart rate variables, absolute HF variability was closely associated with wedge pressure, right atrial and pulmonary arterial pressure, left ventricular ejection fraction and volume, ratio of maximal velocity of early (E) and atrial (A) mitral flow waves, left atrial diameter, plasma norepinephrine, and atrial natriuretic peptide (0.45 < r < 0.65, all P < 0.001). In tachycardia-induced heart failure, absolute HF heart rate variability is a more reliable indicator of cardiac dysfunction and neurohumoral activation than LF heart rate variability.     

川崎病患儿的心率变异性指标与血清NT-proBNP及cTnI水平的相关性

目的:研究川崎病患儿的心率变异性指标与血清氨基末端脑钠肽前体(NT-pro BNP)及肌钙蛋白I(cTnI)水平的相关性,为临床诊疗提供依据。方法:选取2013年7月到2015年7月我院收治的川崎病患儿120例为研究组,根据患者是否存在冠状动脉损害分为A组(有冠状动脉损害)60例和B组(无冠状动脉损害)60例,同时选取同期健康体检儿童60例为对照组,比较各组窦性N-N间期标准差(SDNN)、5min N-N间期平均值标准差(SDANN)、极低频功率(VLF)、低频功率(LF)、高频功率(HF)、NT-proBNP水平以及cTnI水平。结果:研究组SDNN、SDANN、VLF、LF以及HF显著低于对照组,且A组显著低于B组,差异具有统计学意义(P0.05);研究组NT-proBNP水平和cTnI水平显著高于对照组,且A组显著高于B组,差异具有统计学意义(P0.05);研究组NT-proBNP与SDNN和HF呈负相关关系(P0.05),cTnI与SDNN和HF呈负相关关系(P0.05)。结论:心率变异性指标与川崎病患儿冠状动脉损害有关,与NT-proBNP、cTnI呈负相关关系。     

Very low-frequency blood pressure variability depends on voltage-gated L-type Ca2+ channels in conscious rats

The mechanisms generating high- frequency (HF) and low-frequency (LF) blood pressure variability (BPV) are reasonably well understood. However, little is known about the origin of very low-frequency (VLF) BPV. We tested the hypothesis that VLF BPV is generated by L-type Ca(2+) channel-dependent mechanisms. In conscious rats, arterial blood pressure was recorded during control conditions (n = 8) and ganglionic blockade (n = 7) while increasing doses (0.01-5.0 mg.100 micro l(-1).h(-1)) of the L-type Ca(2+) channel blocker nifedipine were infused intravenously. VLF (0.02-0.2 Hz), LF (0.2-0.6 Hz), and HF (0.6-3.0 Hz) BPV were assessed by spectral analysis of systolic blood pressure. During control conditions, nifedipine caused dose-dependent declines in VLF and LF BPV, whereas HF BPV was not affected. At the highest dose of nifedipine, VLF BPV was reduced by 86% compared with baseline, indicating that VLF BPV is largely mediated by L-type Ca(2+) channel-dependent mechanisms. VLF BPV appeared to be relatively more dependent on L-type Ca(2+) channels than LF BPV because lower doses of nifedipine were required to significantly reduce VLF BPV than to reduce LF BPV. Ganglionic blockade markedly reduced VLF and LF BPV and abolished the nifedipine-induced dose-dependent declines in VLF and LF BPV, suggesting that VLF and LF BPV require sympathetic activity to be evident. In conclusion, VLF BPV is largely mediated by L-type Ca(2+) channel-dependent mechanisms. We speculate that VLF BPV is generated by myogenic vascular responses to spontaneously occurring perturbations of blood pressure. Other factors, such as sympathetic nervous system activity, may elicit a permissive effect on VLF BPV by increasing vascular myogenic responsiveness.     

摄食行为对小型猪心脏自主神经功能的影响

目的观察摄食行为对小型猪心脏自主神经功能的影响。方法利用大动物无创遥测技术观察清醒活动状态下小型猪摄食前（BI）、摄食过程中（IP）、摄食后（AI）、AI 2 h和AI 4h的心电图（ECG）和自主活动,并用HRV功率谱分析其自主神经功能。结果与摄食前比较,小型猪摄食过程中心率（HR）、自主活动和标准化低频成分（LFnu）明显增加,RR间期（RRI）、总功率（TP）、极低频成分（VLF）、高频成分（HF）明显减少,LF/HF比值明显升高;且随着摄食后恢复时间的延长,小型猪HR、自主活动、LFnu均有所降低,而RRI、TP、VLF、HF均有所升高,LF/HF比值逐渐降低,并在摄食后2 h、4 h时变化显著;相关分析显示摄食行为与TP、VLF、HF、LF和LF/HF密切相关,多元线性逐步回归分析亦显示摄食行为与VLF、LF/HF和TP密切相关,且VLF起主要作用。结论小型猪摄食行为不仅影响心脏活动;而且能引起小型猪心脏自主神经控制能力发生改变,其中VLF在摄食行为过程中占有重要作用。     

The effect of sinus node depression on heart rate variability in humans using zatebradine, a selective bradycardic agent

Zatebradine is a bradycardic agent with a selective effect on the pacemaker current in the sinus node. The effect of such drugs on heart rate variability is not known. Thirty-six patients without structural heart disease were randomly assigned to receive 10 mg of zatebradine i.v. (n = 24) or isotonic saline (n = 12). Heart rate variability (HRV) was recorded as power in the very low frequency (VLF, 0.003-0.040 Hz), low frequency (LF, 0.040-0.150 Hz), and high frequency (HF, 0.150-0.400 Hz) spectral bands as well as total power (TP, 0.003-0.400 Hz) during 5-min ECG acquisitions at baseline, 30, and 60 min following the start of the infusion. No change in heart rate variability was detected in the control group. Zatebradine significantly reduced heart rate variability at 60 min in all frequency bands: VLF (-12+/-4%, p<0.001), LF (-19+/-4%, p<0.001), and HF (-26+/-5%, p<0.001). The reduction in HRV following zatebradine is due to depression of sinus node response to all external stimuli and underscores the need for documentation of normal sinus node function in HRV research.