基于复杂度的心率变异性分析研究进展

心率变异性（HRV）是当前心电图分析的一个前沿热点,它反映了交感神经和副交感神经对心血管系统的综合调节作用,是评价心血管系统功能的重要指标。随着非线性动力学和复杂性科学的发展,HRV信号被普遍认为是混沌或含有混沌成分的信号。复杂度是用来表征一个心率非线性动力学系统复杂程度的量度,以其简单快速的优点引起了众多研究者的兴趣,并广泛应用于心率变异性分析。本文综述了国内外复杂度算法的研究进展及基于复杂度的心率变异性分析的临床应用及前景。     

豚鼠听神经放电的复杂性分析

运用刻划非线性动力系统复杂性的两种测算方法：复杂度和近似熵,结合替代数据法,研究豚鼠听神经单纤维放电时间间隔序列的复杂性。结果显示,听神经自发放电时间间隔序列的复杂度要高于诱发时的复杂度;听神经诱发放电时间间隔序列的近似熵低于随机重排替代数据的近似熵。提示听神经放电不是完全随机的过程,而可能是混沌的动力学行为,而且诱发放电时的规律性更强。     

基于估计熵确定心率变异信号中动力噪声强度

目前普遍的观点认为心率变异信号是确定性低维混沌系统产生的,同时该系统受到大量生理噪声的影响。研究了观测噪声和动力噪声对低维混沌系统的影响,提出了一种基于复杂性度量动力噪声强度刻划方法,表明随着动力噪声强度的增加,系统的复杂程度增加。该方法不需要对动力学系统完全重建,并对观测噪声具有一定鲁棒性。最后利用３类共５３只狗的心电图,每只狗的心电数据为１０００个Ｒ－Ｒ间期的微分序列检验了该算法。分析表明,估计出的动力噪声强度与不同的心脏功能状态相关联     

用近似熵测量神经放电峰峰间期的复杂性

近似熵是用来测量信号复杂程度的非线性方法。为了研究神经放电序列的复杂性,用该方法及其改进方法对大鼠损伤坐崩神经模型、大鼠脑薄片视上核神经元自发放电模型、背根节自发放电模型峰峰间期以及Rose-Hindmarsh理论神经元模型分叉数据进行了动态测量。结果表明,近似熵可以定量反映多种神经放电序列复杂性的变化,是一种较为有效的复杂性序量方法。     

心肌细胞自发性搏动节律的分岔和混沌现象

心脏的节律是复杂的、非线性的;其节律复杂性的起源是多层次的。实验观察了心肌细胞自发性搏动节律的模式,以及改变细胞间耦合强度时节律的转化规律。表明在以正常灌流液灌流状态下,心肌细胞表现为多种不同的节律模式,可以是周期的,也可以是非周期的。当细胞间耦合强度下降时,心肌细胞节律发生转化,并经倍周期分岔进入混沌节律。实验结果有助于更好地理解心脏节律复杂性的起源。     

Hindmarsh-Rose 神经网络的混沌同步

研究了通过特殊构造的非线性函数耦合连接的神经网络的混沌同步问题。在发展基于稳定性准则的混沌同步方法的基础上,给出了计算同步稳定性的误差发展方程,当耦合强度取参考值时,可实现稳定的混沌同步而不需要计算最大条件Lyapunov指数去判定是否稳定。通过对按照完全连接形式构成的Hindmarsh-Rose神经网络的数值模拟,显示可仅从两个耦合神经的耦合强度的稳定性范围预期到许多耦合神经实现同步的稳定性范围。该方法在噪声影响下,对实现神经元的混沌同步仍具有较强的鲁棒性。此外发现随着耦合神经数的增加,满足同步稳定性的耦合强度减小,与耦合神经的数量成反比。     

健康人不同生理状态下的脑电近似熵的观测

目的：应用近似熵（ＡｐＥｎ）研究不同生理状态下脑电图非线性动力学特性。方法：在一组健康人４０例中,进行五种生理状态的脑电图记录：闭眼安静;睁眼安静;看图;听短纯音;闭眼数数目１００￣７,并计算各种状态的近似熵。结果：闭眼安静状态额区（Ｆ３,Ｆ４）的ＡｐＥｎ最高,枕区（Ｏ１,Ｏ２）最低,睁眼状态所有脑区的ＡｐＥｎ均增高,不同的生理刺激任务对ＥＥＧ ＡｐＥｎ产生不同的影响,其中额区的影响最大。结论：Ａ     

低维非线性呼吸系统的复杂性计算

首先应用混沌计算方法：关联维数D2和最大李亚普努夫指数LLE,以及替代数据分析法,分析了男性受试者在平静状态下记录的呼吸系统时间序列的混沌特征。同时,在呼吸变量的非线性分析中首次引进了被称为C0复杂度的新技术．它的应用将有助于更好地理解自主神经系统中潜在的生理过程。LLE计算的替代数据法分析结果显示,没有明确的证据可以证实受试者在平静状态下的呼吸时序的模态是混沌的。然而,C0复杂度的计算结果却表明大部分呼吸系统的时间序列表现为某种程度的复杂性,这为呼吸模态的非随机变化的属性提供了部分的实验和计算证据。更进一步,C0复杂度有可能以一种新的、确定的方式给出呼吸系统在激励状态下的量化改变。     

基于心电信号的飞行员应激评价模型的研究

本文基于教练机飞行员训练期间的心电信号,以人体瞬间应激水平为评价依据,通过采集特殊的飞行作业期间的飞行员的心电信号,计算心率以及心率变异性的相关指标,对个体产生瞬间应激的心电信号进行心率相关指标分析以及心率变异性的时域指标分析.同时对应激反应下心率曲线面积变化进行分析,采用多尺度算法,构建了应激强度随训练次数变化的函数关系,揭示了飞行训练应激强度变化的规律,提出了飞行训练及应激阶段的划分方法,建立了基于心电信号的飞行员应激评价的模型.     

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     

Fetal heart rate variability and brain stem injury after asphyxia in preterm fetal sheep

This study was undertaken to determine the mechanisms mediating changes in fetal heart rate variability (FHRV) during and after exposure to asphyxia in the premature fetus. Preterm fetal sheep at 0.6 of gestation (91 +/- 1 days, term is 147 days) were exposed to either sham occlusion (n = 10) or to complete umbilical cord occlusion for either 20 (n = 7) or 30 min (n = 10). Cord occlusion led to a transient increase in FHRV with abrupt body movements that resolved after 5 min. In the 30 min group there was a marked increase in FHRV in the final 10 min of occlusion related to abnormal atrial activity. After reperfusion, FHRV in both study groups was initially suppressed and progressively increased to baseline levels over the first 4 h of recovery. In the 20 min group this improvement was associated with return of normal EEG activity and movements. In contrast, in the 30 min group the EEG was abnormal with epileptiform activity superimposed on a suppressed background, which was associated with abnormal fetal movements. As the epileptiform activity resolved, FHRV fell and became suppressed for the remainder of the study. Histological assessment after 72 h demonstrated severe brain stem injury in the 30 min group but not in the 20 min group. In conclusion, during early recovery from asphyxia, epileptiform activity and associated abnormal fetal movements related to evolving neural injury can cause a confounding transient increase in FHRV, which mimics the normal pattern of recovery. However, chronic suppression of FHRV was a strong predictor of severe brain stem injury.     

Paeonol alleviates primary dysmenorrhea in mice via activating CB2R in the uterus

Background and purposePrimary dysmenorrhea is the most common gynaecologic problem in menstruating women and is characterized by spasmodic uterine contraction and pain symptoms associated with inflammatory disturbances. Paeonol is an active phytochemical component that has shown anti-inflammatory and analgesic effects in several animal models. The aim of this study was to explore whether paeonol is effective against dysmenorrhea and to investigate the potential mechanism of cannabinoid receptor signalling.Experimental approachDysmenorrhea was established by injecting oestradiol benzoate into female mice. The effects of paeonol on writhing time and latency, uterine pathology and inflammatory mediators were explored. Isolated uterine smooth muscle was used to evaluate the direct effect of paeonol on uterine contraction.Key resultsThe oral administration of paeonol reduced dysmenorrhea pain and PGE2 and TNF-α expression in the uterine tissues of mice, and paeonol was found to be distributed in lesions of the uterus. Paeonol almost completely inhibited oxytocin-, high potassium- and Ca²⁺-induced contractions in isolated uteri. Antagonists of CB2R (AM630) and the MAPK pathway (U0126), but not of CB1R (AM251), reversed the inhibitory effect of paeonol on uterine contraction. Paeonol significantly blocked L-type Ca²⁺ channels and calcium influx in uterine smooth muscle cells via CB2R. Molecular docking results showed that paeonol fits well with the binding site of CB2R.Conclusions and implicationsPaeonol partially acts through CB2R to restrain calcium influx and uterine contraction to alleviate dysmenorrhea in mice. These results suggest that paeonol has therapeutic potential for the treatment of dysmenorrhea.     

Substance P and calcitonin gene-related peptide immunoreactivity in nerves of the rat uterus: localization, colocalization and effects on uterine contractility.

Immunoreactivity to the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) was examined in nerves in the rat uterus as a prelude to studying their effects on uterine contractility. With immunocytochemical techniques, SP immunoreactivity (SP-I) and CGRP-I were localized in myometrial nerves throughout the uterine horns, with nerves immunoreactive for CGRP being the more numerous. Immunocytochemical double labeling studies revealed SP coexisted with CGRP in a subpopulation of CGRP-I nerve fibers, i.e., SP-I was not present in all CGRP-I nerves. Effects of these neuropeptides on uterine contractility were examined on in vitro preparations of uterine horns from diethylstilbestrol-treated rats. SP (10(-4) to 10(-8) M) stimulated uterine contraction in a dose-related manner. CGRP(1-37) and CGRP(8-37) had no effect on basal uterine tension. While CGRP(1-37) (10(-7) M) reduced SP-stimulated (10(-5) M) uterine contraction by 56%, CGRP(8-37) had no effect on SP-stimulated uterine contraction. However, CGRP(8-37) (10(-6) M) significantly reduced the ability of CGRP(1-37) (10(-7) M) to inhibit SP-stimulated uterine contraction. These results demonstrate that SP- and CGRP-I are present in, and coexist in some uterine nerves, presumably afferent nerves. The first 7 amino acids are necessary for the inhibitory effect of CGRP(1-37) on stimulated uterine contraction. In addition, CGRP(8-37) acted as an antagonist to this inhibitory action. SP and CGRP could be coreleased from afferent fibers in an "efferent fashion" and influence uterine contractility. SP having a contractile effect and CGRP having a relaxing effect.     

Adrenergic influence of uterine muscle contractions stimulated by a glycoside from the root of Dalbergia saxatilis

The mechanism of uterine muscle contraction stimulated by a triterpenoid glycoside (dalsaxin) isolated from the root of D. saxatilis was investigated by in vitro methods in the rat. Dalsaxin caused a dose-related increase in uterine muscle contraction. The contraction was single and transient and was abolished by moderate doses of isoprenaline (1.80 nmol-0.40 mumol) and salbutamol (0.13-25 mumol). Adrenaline (9.10 nmol) also caused a reversible decrease (92.6%; P < 0.01) in myometrial contraction stimulated by this glycoside (0.24 mg/ml). Uterine muscle responses to dalsaxin (0.24 mg/ml) were enhanced by the beta-adrenergic receptor antagonist, propranolol, in a dose related manner. Atipamezole (1.50 ng/ml) but not prazosin (7.72 nmol-15.60 nmol) substantially reduced (80%; P < 0.01) myometrial contractions induced by this uterine spasmogen. The results suggest that dalsaxin enhances uterine muscle contraction by stimulating post junctional alpha 2-adrenergic receptors, presumably by inhibiting plasma membrane adenylate cyclase system and its associated increase in intracellular cAMP content.     

Effects of bPTH fragments (1-34), (3-34) and (7-34) on uterine contraction

Synthetic bovine parathyroid hormone containing the NH2 terminal 34 amino acids [bPTH-(1-34)] was recently demonstrated to inhibit oxytocin stimulated uterine contraction in vitro. The parathyroid hormone analogues [Nle8, Nle18, Tyr34]bPTH-(3-34)amide [NTA-(3-34)] and [Tyr34]bPTH-(7-34)amide [NTA-(7-34)] have been reported to act as inhibitors of antagonists of parathyroid hormone (PTH) in numerous assays. In the present study the effects of these PTH analogues on uterine contraction and the ability of these analogues to act as antagonists to the uterine inhibitory action of bPTH-(1-34) in vitro were investigated. The NTA-(3-34) fragment had no effect on oxytocin stimulated uterine contractions. However, the NTA-(3-34) fragment was able to alter the ability of bPTH (1-34) to reduce oxytocin stimulated uterine contraction in a dose-related manner. Bovine PTH(1-34) (0.3 microgram/ml) reduced the contractile response obtained with oxytocin (0.5 mU/ml) by 20%. A dose of 15 micrograms/ml) of NTA-(3-34) abolished this inhibitory action of bPTH-(1-34) on oxytocin stimulated uterine contraction. In contrast the NTA-(7-34) caused a change in itself, stimulated contraction of resting uterine horns in a dose-related manner; 3.0 micrograms/ml of NTA-(7-34) caused a change in gram tension of + 1.5 grams. Bovine PTH-(1-34) was able to reduce the uterine contraction stimulated by NTA-(7-34) and 0.3 microgram/ml of bPTH-(1-34) reduced the contractile response obtained with 3.0 micrograms/ml of NTA-(7-34) by as much as 70%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of 17-alpha-hydroxy-progesterone capronate on the motility of the human uterus in puerperium following abortion

The effects of 17alpha-hydroxyprogesterone capronate (17-OH-P) on spontaneous uterine motility and on oxytocin-induced uterine contraction during the postabortion period were studied in 22 women. The effects of 17-OH-P were present 8 hours after administration and still appreciable after 12 hours, but were considerably diminished after 24 and 48 hours. The efficiency of 17-OH-P in inhibiting uterine contraction after administration of oxytocin is clearly inferior to that of natural progesterone.     

Inhibition of uterine contraction by synthetic parathyroid hormone fragment

The inhibitory effect of synthetic bovine parathyroid hormone fragment [bPTH-(1-34)] on rat uterine contraction was studied $\text{in vitro}$. Oxytocin, prostaglandin F_2α and acetylcholine produced log dose-related contraction. The addition of bPTH-(1-34) shifted the dose-response curves of the three agonists to the right. Two doses of bPtH-(1-34) were tested. The higher dose (400 ng/ml) caused a greater inhibition of the agonists than did the lower dose (40 ng/ml). bPTH-(1-34) also inhibited the uterine contraction elicited by electrical stimulation of the tissue. We suggest that bPTH-(1-34) has a non-specific depressing effect on the contractile mechanism of the uterine tissue.     

External calcium dependence of the uterine contraction induced by prostaglandins E2 and F2 alpha and its antagonism with natural progestins.

Prostaglandins (PGs) E2 and F2 alpha are strong inducers of uterine contraction by promoting a Ca2+ increase into the cell through specific receptors coupled with the calcium channels. On the contrary, progesterone and 5 beta-reduced progestins promote smooth muscle relaxation by blocking the ion calcium influx. Thus, this study was designed to emphasize the importance of external calcium in the PGs-induced rat uterus contraction. Likewise, also studied was the antagonism and the interaction between PGs and progestins (progesterone and its 5 alpha and 5 beta-reduced derivatives) in the myometrium. Results showed that uterine contraction induced by PGs depends on external calcium, since verapamil or extracellular calcium depletion abolished the PGs effect. Regarding the PGs-progestins antagonism, it was observed that pregnanedione, pregnanolone and epipregnanolone were quite effective for counteracting of PGs-induced contraction. However, progesterone was effective in a middle range, whereas 5 alpha-reduced progestins (allopregnanedione and allopregnanolone) were almost ineffective. It has been concluded that the participation of PGs and progestins in the modulation of uterine contraction might be achieved through the control of calcium influx by opening (PGs) or blocking (progestins) receptor-operated calcium channels.     

Effects of adlay hull extracts on uterine contraction and Ca2+ mobilization in the rat

Dysmenorrhea is directly related to elevated PGF(2alpha) levels. It is treated with nonsteroid antiinflammatory drugs (NSAIDs) in Western medicine. Since NSAIDs produce many side effects, Chinese medicinal therapy is considered as a feasible alternative medicine. Adlay (Coix lachryma-jobi L. var. ma-yuen Stapf.) has been used as a traditional Chinese medicine for treating dysmenorrhea. However, the relationship between smooth muscle contraction and adlay extracts remains veiled. Therefore, we investigated this relationship in the rat uterus by measuring uterine contraction activity and recording the intrauterine pressure. We studied the in vivo and in vitro effects of the methanolic extracts of adlay hull (AHM) on uterine smooth muscle contraction. The extracts were fractionated using four different solvents: water, 1-butanol, ethyl acetate, and n-hexane; the four respective fractions were AHM-Wa, AHM-Bu, AHM-EA, and AHM-Hex. AHM-EA and its subfractions (175 microg/ml) inhibited uterine contractions induced by PGF(2alpha), the Ca(2+) channel activator Bay K 8644, and high K(+) in a concentration-dependent manner in vitro. AHM-EA also inhibited PGF(2alpha)-induced uterine contractions in vivo; furthermore, 375 microg/ml of AHM-EA inhibited the Ca(2+)-dependent uterine contractions. Thus 375 microg/ml of AHM-EA consistently suppressed the increases in intracellular Ca(2+) concentrations induced by PGF(2alpha) and high K(+). We also demonstrated that naringenin and quercetin are the major pure chemical components of AHM-EA that inhibit PGF(2alpha)-induced uterine contractions. Thus AHM-EA probably inhibited uterine contraction by blocking external Ca(2+) influx, leading to a decrease in intracellular Ca(2+) concentration. Thus adlay hull may be considered as a feasible alternative therapeutic agent for dysmenorrhea.     

Dietary Selenium Influences Calcium Release and Activation of MLCK in Uterine Smooth Muscle of Rats

We sought to elucidate the effects of different concentrations of dietary selenium on calcium ion release, MLCK levels, and muscle contraction in the uterine smooth muscle of rats. The selenium (Se) content of blood and of uterine smooth muscle tissues was detected by fluorescence spectrophotometry. Ca²⁺ content was measured by atomic absorption spectroscopy. Calmodulin (CaM) and MLCK RNA and protein levels were analyzed by quantitative real-time polymerase chain reaction and Western blot, respectively. Dietary Se intake increased the Se levels in the blood and in uterine smooth muscle tissues and increased the Ca²⁺ concentration in uterine smooth muscle tissues. The addition of Se also promoted CaM expression and enhanced MLCK activation in uterine smooth muscle tissues. In conclusion, Ca²⁺, CaM, and MLCK were regulated by Se in uterine smooth muscle; Se plays a major role in regulating smooth muscle contraction in the uterus.