Time Course of Heart Rate Variability Decline Following Particulate Matter Exposures in an Occupational Cohort

Although research suggests that particles influence cardiac autonomic response as evidenced by decreases in heart rate variability (HRV), the time course of the response remains unclear. Using a crossover panel study, we monitored 36 male boilermaker welders, occupationally exposed to metal-rich particulate matter (PM) to investigate the temporal trend of hourly HRV subsequent to PM exposure. Ambulatory electrocardiograms were collected over work (exposure) and non-work (control) periods and the mean of the standard deviations of all normal-to-normal intervals for all 5-min segments (SDNN_i) was calculated hourly for up to 14-hrs post-work. The exposure-response relationship was examined with linear mixed effects regression models to account for participants monitored over multiple occasions. Models were adjusted for non-work HRV to control for diurnal fluctuations and individual predictors of HRV. The mean (SD) work PM_{2. 5} concentration was 1.12 (0.76) mg/m³. Hourly SDNN_i was consistently lower post-work as compared to the same time period on a non-work day. HRV was inversely associated with work PM_{2. 5} exposures in each of the 14-hrs post-work. The hourly associations suggested an early and later phase response, with the largest regression coefficients observed 2–3 hrs (β = ?6.86 (95% CI: ?11.91, ?1.81) msec/1 mg/m³ at 3-hrs), and then 9–13 hrs (β = ?8.60 (95% CI: ?17.45, 0.24) msec/1 mg/m³ at 11-hrs), after adjusting for non-work HRV, smoking status, and age. This investigation demonstrates declines in HRV for up to 14 hours following PM exposure and a multiphase cardiovascular autonomic response with immediate (2 hrs) and delayed (9–13 hrs) responses.     

Effects of subchronic exposures to concentrated ambient particles (CAPs) in mice. IV. Characterization of acute and chronic effects of ambient air fine particulate matter exposures on heart-rate variability

Long-term exposure to fine particulate air pollution (PM2.5) has been associated increased risk of death from cardiopulmonary diseases. Cardiac function parameters have also been affected by ambient particulate matter (PM) exposure, including heart-rate variability (HRV), a measure of autonomic function that has been recognized as a well-defined, quantitative indicator of autonomic dysfunction. However, the role of HRV in ambient PM-induced cardiovascular effect is not fully understood. In an accompanying article, we report significant decreasing patterns of heart rate (HR), body temperature, and physical activity for mice lacking apoliproprotein (ApoE-/-) over 5 mo of exposure to concentrated ambient PM (CAPs), with smaller and nonsignificant change for C57 mice. In this article, we report the effects of subchronic CAPs exposure on HRV parameters that are sensitive to cardiac sympathetic and parasympathetic nerve activity. The standard deviation of normal to normal beat intervals (SDNN) and the square root of the mean squared differences of successive RR intervals (RMSSD) in the late afternoon and overnight for the ApoE-/- mice showed a gradual increase for the first 6 wk, a decline for about 12 more wk, and a slight turn upward at the end of the study period. For C57 mice, there were no chronic effect changes of SDNN or RMSSD in the late afternoon, an a slight increase after 6 wk for the overnight period. The response patterns of ApoE-/- mice indicated a perturbation of the homeostatic function in the cardiovascular system (initial enhancement and late depression of the HRV parameters). Our results complement the findings in human panel and controlled CAPs exposure studies in demonstrating that increased levels of particle pollution are able to perturb cardiac autonomic function, which may lead to adverse cardiovascular outcomes.     

Ultrafine carbon black disturbs heart rate variability in mice

Previous epidemiological and toxicological studies have reported the associations between ambient particulate matter (PM) exposure and changes in heart rate variability (HRV), a marker of cardiac autonomic nervous system (ANS) function. However, both the responsible components in PM and their mechanisms affecting HRV remain uncertain. We propose that carbon black (CB), one of the main components in PM, may affect HRV through mechanisms independent of cardio-pulmonary and systemic inflammation and/or injury. Male C57BL/6 mice were exposed by intra-tracheal instillation to ultrafine CB (once every two days for three times) at doses of 0, 0.05, 0.15 and 0.6 mg/kg. HRV indices, standard deviation of all normal R-R intervals (SDNN) and the square root of mean of sum of squares of differences between adjacent normal R-R intervals (RMSSD), showed significant decreases in 0.15 and 0.6 mg/kg CB exposed groups. Slight pulmonary inflammation and myocardial injury were only observed in 0.6 mg/kg CB exposed group. We conclude that CB can disturb cardiac ANS function in mice, indicated by the withdrawal of parasympathetic modulation, through mechanisms independent of apparent myocardial and pulmonary injury.     

Effects of Subchronic Exposures to Concentrated Ambient Particles (CAPs) in Mice: IV. Characterization of Acute and Chronic Effects of Ambient Air Fine Particulate Matter Exposures on Heart-Rate Variability

Abstract

Long-term exposure to fine particulate air pollution (PM_2.5) has been associated with increased risk of death from cardiopulmonary diseases. Cardiac function parameters have also been affected by ambient particulate matter (PM) exposure, including heart-rate variability (HRV), a measure of autonomic function that has been recognized as a well-defined, quantitative indicator of autonomic dysfunction. However, the role of HRV in ambient PM-induced cardiovascular effects is not fully understood. In an accompanying article, we report significant decreasing patterns of heart rate (HR), body temperature, and physical activity for mice lacking apoliproprotein (ApoE^?/?) over 5 mo of exposure to concentrated ambient PM (CAPs), with smaller and nonsignificant changes for C57 mice. In this article, we report the effects of subchronic CAPs exposure on HRV parameters that are sensitive to cardiac sympathetic and parasympathetic nerve activity. The standard deviation of normal to normal beat intervals (SDNN) and the square root of the mean squared differences of successive RR intervals (RMSSD) in the late afternoon and overnight for the ApoE^?/? mice showed a gradual increase for the first 6 wk, a decline for about 12 more wk, and a slight turn upward at the end of the study period. For C57 mice, there were no chronic effect changes of SDNN or RMSSD in the late afternoon, and a slight increase after 6 wk for the overnight period. The response patterns of ApoE^?/? mice indicated a perturbation of the homeostatic function in the cardiovascular system (initial enhancement and later depression of the HRV parameters). Our results complement the findings in human panel and controlled CAPs exposure studies in demonstrating that increased levels of particle pollution are able to perturb cardiac autonomic function, which may lead to adverse cardiovascular outcomes.     

PM2.5-induced changes in cardiac function of hypertensive rats depend on wind direction and specific sources in Steubenville, Ohio

BACKGROUND: Increases in particulate matter less than 2.5 μm (PM(2.5)) in ambient air is linked to acute cardiovascular morbidity and mortality. Specific components and potential emission sources of PM(2.5) responsible for adverse health effects of cardiovascular function are unclear. Methods: Spontaneously hypertensive rats were implemented with radiotelemeters to record ECG responses during inhalation exposure to concentrated ambient particles (CAPs) for 13 consecutive days in Steubenville, OH. Changes in heart rate (HR) and its variability (HRV) were compared to PM(2.5) trace elements in 30-min time frames to capture acute physiological responses with real-time fluctuations in PM(2.5) composition. Using positive matrix factorization, six major source factors were identified: (i) coal/secondary, (ii) mobile sources, (iii) metal coating/processing, (iv) iron/steel manufacturing, (v) lead and (vi) incineration. Results: Exposure-related changes in HR and HRV were dependant on winds predominately from either the northeast (NE) or southwest (SW). During SW winds, the metal processing factor was associated with increased HR, whereas factors of incineration, lead and iron/steel with NE winds were associated with decreased HR. Decreased SDNN was dominated during NE winds by the incinerator factor, and with SW winds by the metal factor. Metals and mobile source factors also had minor impacts on decreased SDNN with NE winds. Individual elemental components loaded onto these factors generally showed significant associations, although there were some discrepancies. Conclusions: Acute cardiovascular changes in response to ambient PM(2.5) exposure can be attributed to specific PM constituents and sources linked with incineration, metal processing, and iron/steel production.     

Heart-rate variability in the apolipoprotein E knockout transgenic mouse following exposure to Seattle particulate matter

Epidemiological studies show that the elderly and/or people with preexisting cardiovascular disease (CVD) are more susceptible to the adverse effects of ambient air pollution. Heart-rate variability (HRV) measured through electrocardiogram (ECG) is a sensitive and effective tool for monitoring the adverse effects of particulate matter (PM). Common HRV parameters used include the standard deviation of the interval between normal beats (SDNN), square root of the mean of the squared differences between normal beats (rMSSD), and distinct high, low, and very low components of frequency. Aged apolipoprotein E knockout transgenic mice, a model of CVD, were implanted with miniaturized ECG telemetry devices and intranasally exposed to saline, 50 microg Seattle PM(2.5) (PM having a mean aerodynamic diameter of < or = 2.5 microm), or silica. They were monitored for a 1-d baseline prior to and for 4 d following exposure. After an initial increase in both heart rate and activity in all groups, there was delayed bradycardia with no change in activity of the animals in the PM- and silica-exposed groups. In addition, with PM and silica exposure there was a decrease in HRV parameters, suggesting a decrease in parasympathetic tone, which may lead to cardiac arrhythmia and mortality. Seattle PM is a toxic species that modulates the autonomic nervous system in a mouse model of CVD.     

Variation in heart rate regulation and the effects of particle exposure in inbred mice

Altered autonomic control of heart rate (HR) rhythm during exposure to particulate matter (PM) has been suggested in human and animal studies. Our lab has shown strain variation in HR regulation between quiescent C3H/HeJ (C3) and C57BL/6J (B6) mice: that is, C3 mice show a consistently higher HR by approximately 80 bpm compared with B6 mice during a normal 24-h circadian cycle. In the current study, we hypothesize that the balance between sympathetic and parasympathetic control of HR during PM exposure varies between C3 and B6 mice. Radiotelemeters were implanted in C3 and B6 mice to measure HR responses and HR variability (HRV) parameters during successive 3-h exposures to filtered air (FA) or carbon black (CB, < 300 mug/m3). Exposures were repeated following administration of saline or parasympathetic (PS; atropine, 0.5 mg/kg i.p.) and sympathetic (S; propranolol, 1 mg/kg i.p.) blockade to study the autonomic regulation of HR during CB exposure. During FA exposure with saline, a significantly (p < .05) greater 3-h average HR response (bpm +/- SEM) occurred in C3 compared with B6 mice (496 +/- 22 vs. 427 +/- 3). With PS blockade, the strain difference between C3 and B6 mice was not evident (485 +/- 23 vs. 503 +/- 61). With S blockade, the 3-h average HR responses for C3 mice were significantly (p < .05) reduced compared with saline (413 +/- 18 vs. 392 +/- 15 for B6). During CB exposure with saline, HR responses were again significantly (p < 0.05) elevated in C3 compared with B6 mice, but these HR responses were not different relative to FA exposure. With S blockade, HR was significantly (p < .05) elevated in B6 mice during CB relative to FA, but was unchanged in C3 mice. Collectively, these results suggest that strain variation in HR regulation is due to a robust PS tone evident in B6 mice and a predominant S tone in C3 mice. Furthermore, CB exposure alters HR regulation in B6 mice by modulating a withdrawal of PS tone. Finally, strain variation in HR between B6 and C3 mice in responding to acute PM exposure implies that robust genetic determinants modulate altered autonomic regulation in susceptible individuals.     

Whole and particle-free diesel exhausts differentially affect cardiac electrophysiology, blood pressure, and autonomic balance in heart failure-prone rats

Epidemiological studies strongly link short-term exposures to vehicular traffic and particulate matter (PM) air pollution with adverse cardiovascular (CV) events, especially in those with preexisting CV disease. Diesel engine exhaust is a key contributor to urban ambient PM and gaseous pollutants. To determine the role of gaseous and particulate components in diesel exhaust (DE) cardiotoxicity, we examined the effects of a 4-h inhalation of whole DE (wDE) (target PM concentration: 500 μg/m(3)) or particle-free filtered DE (fDE) on CV physiology and a range of markers of cardiopulmonary injury in hypertensive heart failure-prone rats. Arterial blood pressure (BP), electrocardiography, and heart rate variability (HRV), an index of autonomic balance, were monitored. Both fDE and wDE decreased BP and prolonged PR interval during exposure, with more effects from fDE, which additionally increased HRV triangular index and decreased T-wave amplitude. fDE increased QTc interval immediately after exposure, increased atrioventricular (AV) block Mobitz II arrhythmias shortly thereafter, and increased serum high-density lipoprotein 1 day later. wDE increased BP and decreased HRV root mean square of successive differences immediately postexposure. fDE and wDE decreased heart rate during the 4th hour of postexposure. Thus, DE gases slowed AV conduction and ventricular repolarization, decreased BP, increased HRV, and subsequently provoked arrhythmias, collectively suggesting parasympathetic activation; conversely, brief BP and HRV changes after exposure to particle-containing DE indicated a transient sympathetic excitation. Our findings suggest that whole- and particle-free DE differentially alter CV and autonomic physiology and may potentially increase risk through divergent pathways.     

氧疗对慢性阻塞性肺疾病患者心率变异性的影响

目的探讨慢性阻塞性肺疾病患者的心率变异性的变化,氧疗对心率变异性的影响及其临床意义。方法选择我院慢性阻塞性肺疾病缓解期患者162例,经肺功能检测分为I级（1组）、Ⅱ级（2组）、Ⅲ级（3组）及Ⅳ级（4组）,均行24h心率变异性监测,检查心率变异性时域指标：24h内窦性心搏RR间期的总体标准差（SDNN）、24h内连续每5min正常RR间期均值的标准差（SDANN）、24h连续每5min节段正常RR间期标准差（SDNNIndex）、24h内相邻正常连续性RR间期差值的均方根（rMSSD）,检查完后给予低流量（1～2L／min）鼻塞吸氧,每天吸氧时间12h以上,1周后再次行心率变异性检测。对比分析四组患者吸氧前后的SDNN、SDNNIndex、SDANN、rMSSD的变化。结果四组患者吸氧前后二氧化碳分压（PCO2）、氧分压（PO2）及pH均无统计学差异（P〉0．05）。四组患者吸氧前,3、4组与1、2组各心率变异性指标比较,差异有统计学意义（P〈0．05）,且随着COPD级别的加重,SDNN、SDNNIndex、SDANN、rMSSD的数值有减小趋势;四组患者吸氧后SDNN、SDNNIndex、SDANN、rMSSD较吸氧前升高,差异有统计学意义（P〈0．05）。结论随着慢性阻塞性肺疾病患者病情加重,心率变异性各时域指标下降,吸氧后心率变异性各指标较吸氧前升高,提示慢性阻塞性肺疾病患者存在自主神经功能损伤,氧疗可能减少自主神经功能的损伤。     

The relationship between air pollutants and heart-rate variability among community residents in Korea

Air pollution, both particulate and gaseous, is known to cause adverse health effects and is associated with increased cardiovascular mortality and morbidity. With a growing recognition in the importance of the autonomic nervous system in air pollution, we examined the effects of air pollutants, namely, particulate matter (PM10), sulfur dioxide (SO2), and nitric dioxide (NO2), on cardiac autonomic function by measuring heart-rate variability (HRV) among community residents. This study was conducted at Taein Island, located off the southern coast of South Korea; 1349 subjects (596 males and 753 females) were included in this analysis. Subjects responded to the interview about general characteristics and an HRV examination was conducted. Exposure data were collected from the Environmental Management Corporation during the same period of HRV measurement. Linear regression analyses were carried out to evaluate the association over 72 h, and the parameters of HRV indices were presented as the percentage change. The exposures to PM(10), SO(2), and NO2 were associated with reduced HRV indices, and significant decreases in the standard deviation of the normal to normal interval (SDNN) and low frequency (LF) domain effect, and the effect was largely continued until 12 h. Our results suggest that air pollutants stimulate the autonomic nervous system and provoke an imbalance in cardiac autonomic control. Thus, these subclinical effects may lead to pathological consequences, particularly in high-risk patients and susceptible subjects.     

阿托伐他汀对心肌梗死患者心率变异性的影响

目的:观察阿托伐他汀对急性心肌梗死(AMI)患者和陈旧性心肌梗死(OMI)患者心率变异性(HRV)的影响。方法:AMI和OMI患者各48例均随机分为试验组和对照组,每组各24例,试验组在常规治疗基础上加用阿托伐他汀10～20 mg·d-1,qd,疗程4周。对照组仅采用常规治疗(酒石酸美托洛尔12．5～50 mg,bid,硝酸异山梨酯5～10 mg,tid)。治疗前后用数字化24 h Holter记录测定心率变异性时域参数(SDNN)和频域参数(LF和HF)。结果:AMI患者试验组治疗4周后,HRV各项指标均明显好转,SDNN,LF和HF均明显增加,LF／HF明显降低,与治疗前比较和组间比较差异均有显著性(P<0．05)。OMI患者试验组SDNN与治疗前比较及组间比较无明显变化(P>0．05),LF和HF均明显增加,LF／HF明显降低,与治疗前比较和组间比较差异有显著性(P<0．05)。结论:阿托伐他汀具有降低心肌梗死患者交感神经活性,提高迷走神经张力的作用,使LF／HF趋于正常,提示该药具有稳定AMI患者自主神经功能的作用。     

The relationship between traffic-related air pollutants and cardiac autonomic function in a panel of healthy adults: a further analysis with existing data

Context: Epidemiological studies have linked particulate matter (PM) and carbon monoxide (CO) exposures with alterations in cardiac autonomic function as measured by heart rate variability (HRV) in populations. Recently, we reported association of several HRV indices with marked changes in particulate air pollution around the Beijing 2008 Olympic Games in a panel of healthy adults.

Objective: We further investigated the cardiac effects of traffic-related air pollutants over wide exposure ranges with expanded data set in this panel of healthy adults.

Methods: We obtained real-time data on nine taxi drivers’ in-car exposures to PM ≤2.5?µm in aerodynamic diameter (PM_2.5) and CO and on multiple HRV indices during a separate daily work shift in four study periods with dramatically changing air pollution levels around the Beijing 2008 Olympic Games. Mixed effect models and a loess smoother method were used to investigate the associations of exposures with HRV indices.

Results: Results showed overall negative associations of traffic-related air pollutants with HRV indices across periods, as well as differences in period-specific and individual associations. After stratifying the individuals into two different response groups (positive/negative), cardiac effects of air pollutants became stronger within each group. Exposure–response modeling identified changed curvilinear relationships between air pollution exposures and HRV indices with threshold effects.

Discussion and conclusion: Our results support the association of exposure to traffic-related air pollution with altered cardiac autonomic function in young healthy adults free of cardiovascular compromises. These results suggest a complicated mechanism that traffic-related air pollutants influence the cardiovascular system of healthy adults.     

Docetaxel does not impair cardiac autonomic function in breast cancer patients previously treated with anthracyclines

The effects of docetaxel treatment on autonomic cardiac function was studied with 24-h ECG recordings in breast cancer patients pretreated with anthracyclines. Twenty-four women were evaluated before docetaxel treatment and after 3-4 courses of docetaxel 100 mg/m(2). The heart rate, cardiac extrasystoles and heart rate variability (HRV) in both the time and frequency domain were assessed from 24-h ECG recordings. The acute effects of docetaxel were calculated from 1-h recordings immediately prior to, during and after infusion. Long-term effects were evaluated from 24-h recordings performed before treatment and after 3-4 courses of docetaxel. There was no increase in the number of cardiac extrasystoles during docetaxel infusion. The number of ventricular extrasystoles decreased from 14 (23) to 7 (14) during and 5 (10) after the first infusion (p=0.02). The heart rate, HRV and extrasystoles were similar before and after 3-4 courses of docetaxel. The treatment did not abolish circadian variability of the heart rate. Docetaxel did not deteriorate autonomic cardiac function. In conclusion, our findings suggest that docetaxel does not have harmful cumulative effects on autonomic control of the heart and is therefore unlikely to be cardiotoxic.     

Particulate matter inhalation exacerbates cardiopulmonary injury in a rat model of isoproterenol-induced cardiomyopathy

Ambient particulate matter (PM) exposure is linked to cardiovascular events and death, especially among individuals with heart disease. A model of toxic cardiomyopathy was developed in Spontaneously Hypertensive Heart Failure (SHHF) rats to explore potential mechanisms. Rats were infused with isoproterenol (ISO; 2.5?mg/kg/day subcutaneous [sc]), a β-adrenergic agonist, for 28 days and subsequently exposed to PM by inhalation. ISO induced tachycardia and hypotension throughout treatment followed by postinfusion decrements in heart rate, contractility, and blood pressures (systolic, diastolic, pulse), and fibrotic cardiomyopathy. Changes in heart rate and heart rate variability (HRV) 17 days after ISO cessation indicated parasympathetic dominance with concomitantly altered ventilation. Rats were subsequently exposed to filtered air or Harvard Particle 12 (HP12) (12?mg/m³)—a metal-rich oil combustion-derived PM—at 18 and 19 days (4?h/day) after ISO infusion via nose-only inhalation to determine if cardio-impaired rats were more responsive to the effects of PM exposure. Inhalation of PM among ISO-pretreated rats significantly increased pulmonary lactate dehydrogenase, serum high-density lipoprotein (HDL) cholesterol, and heart-to-body mass ratio. PM exposure increased the number of ISO-pretreated rats that experienced bradyarrhythmic events, which occurred concomitantly with acute alterations of HRV. PM, however, did not significantly affect mean HRV in the ISO- or saline-pretreated groups. In summary, subchronic ISO treatment elicited some pathophysiologic and histopathological features of heart failure, including cardiomyopathy. The enhanced sensitivity to PM exposure in SHHF rats with ISO-accelerated cardiomyopathy suggests that this model may be useful for elucidating the mechanisms by which PM exposure exacerbates heart disease.     

培哚普利对2型糖尿病合并心脑血管疾病心率变异性的影响

目的　研究血管紧张素转换酶抑制剂培哚普利 (perindopril)对 2型糖尿病合并心脑血管疾病患者心率变异性 (heart rate variability,HRV)的影响。方法　 35例 2型糖尿病合并心脑血管疾病者服培哚普利 (4～6 mg/ d,8周 ) ,前后行 2 4 h动态心电图检查 ,分析心率功率谱时域和频域指标。结果　培哚普利使 HRV时域指标正常 RR间期的标准差 (SDNN)、每连续 5 min时段标准差 (SDANN) ,相邻 RR间期之差的均方根值 (r MSSD)和频域指标高频 (HF)显著增加 ,频域指标总频谱 (TF) ,低频 (L F)和 L F/ HF明显降低。结论　培哚普利对糖尿病合并心脑血管疾病患者心率变异性产生有益的作用 ,并对预防心脑血管疾病再发有重要意义     

Electrocardiographic and respiratory responses to coal-fired power plant emissions in a rat model of acute myocardial infarction: results from the Toxicological Evaluation of Realistic Emissions of Source Aerosols Study

BACKGROUND: Ambient particulate matter (PM) derived from coal-fired power plants may have important cardiovascular effects, but existing toxicological studies are inadequate for understanding these effects. The Toxicological Evaluation of Realistic Emissions of Source Aerosols (TERESA) study aims to evaluate the toxicity of primary and secondary PM derived from coal-fired power plants. As a part of this effort, we evaluated in susceptible animals the effect of stack emissions on cardiac electrophysiology and respiratory function under exposure conditions intended to simulate an aged plume with unneutralized acidity and secondary organic aerosols (POS exposure scenario). METHODS: Rats with acute myocardial infarction were exposed to either stack emissions (n = 15) or filtered air (n = 14) for 5 h at a single power plant. Respiration and electrocardiograms were continuously monitored via telemetry and heart rate, heart rate variability (HRV), premature ventricular beat (PVB) frequency, electrocardiographic intervals, and respiratory intervals and volumes were evaluated. Similar experiments at another power plant were attempted but were unsuccessful. Results: POS exposure (fine particle mass = 219.1 μg/m(3); total sulfate = 172.5 μg/m(3); acidic sulfate = 132.5 μg/m(3); organic carbon = 50.9 μg/m(3)) was associated with increased PVB frequency and decreased respiratory expiratory time and end-inspiratory pause, but not with changes in heart rate, HRV, or electrocardiographic intervals. Results from a second power plant were uninterpretable. Conclusions: Short-term exposure to primary and unneutralized secondary PM formed from aged emissions from a coal-fired power plant, as simulated by the POS scenario, may be associated with increased risk of ventricular arrhythmias in susceptible animals.     

缬沙坦对高血压及心率变异性影响的研究

目的:研究缬沙坦对高血压心率变异性的影响。方法:选择80例原发性高血压患者服用缬沙坦,分别在治疗前与治疗14周后进行动态心电图(DCG)及心率变异性(HRV)检查,并与对照组(40例)进行比较。结果:治疗后连续R-R间期标准差(SDNN),相邻R-R均方差(RMSSD),相邻R-R间期大于50ms百分数(PNN50)、高频功率(HF)值均明显上升;低频功率与高频功率比值(LF/HF)显著降低(P<0.01),结论:原发性高血压患者存在HRV下降,而缬沙坦在降压的同时,可提高HRV,改善自主神经功能失调。     

Particle effects on heart-rate regulation in senescent mice

Because epidemiology studies consistently identify the elderly at risk for air pollution-related morbidity and mortality, we developed a model of senescent-dependent susceptibility based on indices of physiological aging. In the current study, we hypothesized that heart-rate regulation during particulate matter (PM) exposure differs with senescence-dependent susceptibility owing to variation in autonomic nervous control. Heart rate (HR) and heart-rate variability (HRV) parameters were measured from 162 samples of 2-min electrocardiograph (ECG) recordings in age-matched healthy (n = 5) and terminally senescent (n = 3) AKR mice during 3-h exposures to filtered-air (FA, day 1) and carbon black (CB, day 4; <200 microg/m(3)). On day 1, HR was significantly (p <.01) depressed during FA in terminally senescent mice. By day 4, HR was further slowed significantly (p <.01) due to the effects of CB exposure for 3 days. The combined effects of terminal senescence and CB exposure acted to depress HR to an average (+/-SEM) 445 +/- 40 bpm, or approximately 80 bpm lower compared to healthy HR responses. The change in rMSSD, an HRV parameter corresponding to relative influences of parasympathetic tone on HR, was significantly (p <.01) greater on day 1 and day 4 in terminally senescent mice compared to healthy mice. In contrast, the LF/HF ratio, an HRV parameter derived from spectral analysis indicating relative changes in cardiac sympathetic tone, was significantly (p <.01) depressed in terminally senescent mice on day 1. By day 4, significant increases in LF/HF were evident in healthy mice during CB exposure, suggesting that HR regulation was associated with an increase in sympathetic tone. Alternatively, terminally senescent mice appeared to modulate a lower HR without change in LF/HF ratio during CB exposure, suggesting an absence of sympathetic tone. In conclusion, older healthy mice increase cardiac sympathetic tone during PM exposure while terminally senescent mice show a greater PM-induced parasympathetic tone in regulating HR. The significance of the current results suggest that PM-induced HR regulatory changes may ultimately depend on the degree of physiological aging.     

Further evaluation of the kinetics of white spirit in human volunteers

This paper gives supplementary informations on the kinetics of aliphatic white spirit in humans. Eight volunteers were exposed to 600 mg/m3 (100 p.p.m.) white spirit during 3 hrs. Calculated pulmonary uptake (dose) was 392 +/- 38 mg, residence time 47.5 hrs, volume of distribution 749 1, and total body clearance 263 ml/min. Then 7 volunteers were exposed to 600 mg/m3 white spirit 6 hrs daily in 5 consecutive days. Calculated pulmonary uptake was 3464 +/- 329 mg. A mathematic model is presented which uses the blood concentrations to calculate the tissue concentrations during repeated doses administered over an extended period. By means of this model and the measured concentrations in blood and fat, the partition coefficient fat: blood for white spirit was calculated to 47. Estimated redistribution phase of white spirit in adipose tissue was approximately 20 hrs for the first 5 exposures, and half-life in adipose tissue after redistribution 46-48 hrs. During exposure to 600 mg/m3 white spirit 6 hrs daily, 5 days a week, calculated maximum steady state concentrations were 55 mg/kg fat and 5 mg/kg brain, minimum steady state concentrations 35 mg/kg fat and 0.6 mg/kg brain. These values for half-life and steady-state concentrations are considered more correct than our previously reported values, which did not take into account the existence of a redistribution phase.     

PM2.5-induced changes in cardiac function of hypertensive rats depend on wind direction and specific sources in Steubenville,Ohio

Background: Increases in particulate matter less than 2.5?µm (PM_2.5) in ambient air is linked to acute cardiovascular morbidity and mortality. Specific components and potential emission sources of PM_2.5 responsible for adverse health effects of cardiovascular function are unclear.

Methods: Spontaneously hypertensive rats were implemented with radiotelemeters to record ECG responses during inhalation exposure to concentrated ambient particles (CAPs) for 13 consecutive days in Steubenville, OH. Changes in heart rate (HR) and its variability (HRV) were compared to PM_2.5 trace elements in 30-min time frames to capture acute physiological responses with real-time fluctuations in PM_2.5 composition. Using positive matrix factorization, six major source factors were identified: (i) coal/secondary, (ii) mobile sources, (iii) metal coating/processing, (iv) iron/steel manufacturing, (v) lead and (vi) incineration.

Results: Exposure-related changes in HR and HRV were dependant on winds predominately from either the northeast (NE) or southwest (SW). During SW winds, the metal processing factor was associated with increased HR, whereas factors of incineration, lead and iron/steel with NE winds were associated with decreased HR. Decreased SDNN was dominated during NE winds by the incinerator factor, and with SW winds by the metal factor. Metals and mobile source factors also had minor impacts on decreased SDNN with NE winds. Individual elemental components loaded onto these factors generally showed significant associations, although there were some discrepancies.

Conclusions: Acute cardiovascular changes in response to ambient PM_2.5 exposure can be attributed to specific PM constituents and sources linked with incineration, metal processing, and iron/steel production.