Alterations In Autonomic Control Research Articles

Exercise training normalizes an increased neuronal excitability of NTS-projecting neurons of the hypothalamic paraventricular nucleus in hypertensive rats

Elevated sympathetic outflow and altered autonomic reflexes, including impaired baroreflex function, are common findings observed in hypertensive disorders. Although a growing body of evidence supports a contribution of preautonomic neurons in the hypothalamic paraventricular nucleus (PVN) to altered autonomic control during hypertension, the precise underlying mechanisms remain unknown. Here, we aimed to determine whether the intrinsic excitability and repetitive firing properties of preautonomic PVN neurons that innervate the nucleus tractus solitarii (PVN-NTS neurons) were altered in spontaneously hypertensive rats (SHR). Moreover, given that exercise training is known to improve and/or correct autonomic deficits in hypertensive conditions, we evaluated whether exercise is an efficient behavioral approach to correct altered neuronal excitability in hypertensive rats. Patch-clamp recordings were obtained from retrogradely labeled PVN-NTS neurons in hypothalamic slices obtained from sedentary (S) and trained (T) Wistar-Kyoto (WKY) and SHR rats. Our results indicate an increased excitability of PVN-NTS neurons in SHR-S rats, reflected by an enhanced input-output function in response to depolarizing stimuli, a hyperpolarizing shift in Na(+) spike threshold, and smaller hyperpolarizing afterpotentials. Importantly, we found exercise training in SHR rats to restore all these parameters back to those levels observed in WKY-S rats. In several cases, exercise evoked opposing effects in WKY-S rats compared with SHR-S rats, suggesting that exercise effects on PVN-NTS neurons are state dependent. Taken together, our results suggest that elevated preautonomic PVN-NTS neuronal excitability may contribute to altered autonomic control in SHR rats and that exercise training efficiently corrects these abnormalities.

Tachycardia in adults with cystic fibrosis is associated with normal autonomic function

Whether autonomic dysfunction contributes to tachycardia in cystic fibrosis (CF) is unknown. Heart rate variability (HRV) was assessed to determine high frequency power and the low/high frequency power ratio (HF, LF/HF) as markers of vagal and sympathovagal balance, respectively, under spontaneous and controlled breathing (15 breaths per minute (bpm)) conditions in 17 CF and 17 healthy control subjects. Under spontaneously breathing conditions, the CF group was tachycardic (75.4 ± 11.2 vs 60.2 ± 9.0 br/min P < 0.001) and tachypnoeic (22.6 ± 5.8 vs 13.6 ± 4.1 br/min, P= 0.001) compared with controls. No significant difference in HRV was observed between groups during spontaneous or controlled breathing. Coexistent diabetes mellitus and β(2) agonist use were not associated with altered autonomic control. During controlled breathing, the CF group showed a negative correlation between forced expiratory volume in 1 s (FEV(1)) % predicted and HF power (P= 0.013, r=-0.59) and a positive correlation between FEV(1) % predicted and LF/HF ratio (P= 0.002, r= 0.69) suggesting an exaggerated normal vagal response. CF patients have normal autonomic function.

Autonomic control of the heart is altered in Sprague-Dawley rats with spontaneous hydronephrosis

The renal medulla plays an important role in cardiovascular regulation, through interactions with the autonomic nervous system. Hydronephrosis is characterized by substantial loss of renal medullary tissue. However, whether alterations in autonomic control of the heart are observed in this condition is unknown. Thus we assessed resting hemodynamics and baroreflex sensitivity (BRS) for control of heart rate in urethane/chloralose-anesthetized Sprague-Dawley rats with normal or hydronephrotic kidneys. While resting arterial pressure was similar, heart rate was higher in rats with hydronephrosis (290 ± 12 normal vs. 344 ± 11 mild/moderate vs. 355 ± 13 beats/min severe; P < 0.05). The evoked BRS to increases, but not decreases, in pressure was lower in hydronephrotic rats (1.06 ± 0.06 normal vs. 0.72 ± 0.10 mild/moderate vs. 0.63 ± 0.07 ms/mmHg severe; P < 0.05). Spectral analysis methods confirmed reduced parasympathetic function in hydronephrosis, with no differences in measures of indirect sympathetic activity among conditions. As a secondary aim, we investigated whether autonomic dysfunction in hydronephrosis is associated with activation of the renin-angiotensin system (RAS). There were no differences in circulating angiotensin peptides among conditions, suggesting that the impaired autonomic function in hydronephrosis is independent of peripheral RAS activation. A possible site for angiotensin II-mediated BRS impairment is the solitary tract nucleus (NTS). In normal and mild/moderate hydronephrotic rats, NTS administration of the angiotensin II type 1 receptor antagonist candesartan significantly improved the BRS, suggesting that angiotensin II provides tonic suppression to the baroreflex. In contrast, angiotensin II blockade produced no significant effect in severe hydronephrosis, indicating that at least within the NTS baroreflex suppression in these animals is independent of angiotensin II.

Aging reduces complexity of heart rate variability assessed by conditional entropy and symbolic analysis

Increasing age is associated with a reduction in overall heart rate variability as well as changes in complexity of physiologic dynamics. The aim of this study was to verify if the alterations in autonomic modulation of heart rate caused by the aging process could be detected by Shannon entropy (SE), conditional entropy (CE) and symbolic analysis (SA). Complexity analysis was carried out in 44 healthy subjects divided into two groups: old (n = 23, 63 ± 3 years) and young group (n = 21, 23 ± 2). It was analyzed SE, CE [complexity index (CI) and normalized CI (NCI)] and SA (0V, 1V, 2LV and 2ULV patterns) during short heart period series (200 cardiac beats) derived from ECG recordings during 15 min of rest in a supine position. The sequences characterized by three heart periods with no significant variations (0V), and that with two significant unlike variations (2ULV) reflect changes in sympathetic and vagal modulation, respectively. The unpaired t test (or Mann-Whitney rank sum test when appropriate) was used in the statistical analysis. In the aging process, the distributions of patterns (SE) remain similar to young subjects. However, the regularity is significantly different; the patterns are more repetitive in the old group (a decrease of CI and NCI). The amounts of pattern types are different: 0V is increased and 2LV and 2ULV are reduced in the old group. These differences indicate marked change of autonomic regulation. The CE and SA are feasible techniques to detect alteration in autonomic control of heart rate in the old group.

Simultaneous parasympathetic and sympathetic activation reveals altered autonomic control of heart rate, vascular tension, and epinephrine release in anesthetized hypertensive rats

Sympathetic hyperactivity and parasympathetic insufficiency characterize blood pressure (BP) control in genetic hypertension. This shift is difficult to investigate in anesthetized rats. Here we present a pharmacological approach to simultaneously provoke sympathetic and parasympathetic transmitter release, and identify their respective roles in the concomitant cardiovascular response. To stimulate transmitter release in anesthetized normotensive (WKY) and spontaneously hypertensive rats (SHR), we injected intravenously 4-aminopyridine (4-AP), a voltage-sensitive K+ channel (KV) inhibitor. A femoral artery catheter monitored BP, an ascending aorta flow-probe recorded cardiac output and heart rate (HR). Total peripheral vascular resistance (TPVR) was calculated. 4-AP-induced an immediate, atropine (muscarinic antagonist)- and hexamethonium (ganglion blocker)-sensitive bradycardia in WKY, and in both strains, a subsequent, sustained tachycardia, and norepinephrine but not epinephrine release. Reserpine (sympatholytic), nadolol (β-adrenoceptor antagonist) or right vagal nerve stimulation eliminated the late tachycardia, adrenalectomy, scopolamine (central muscarinic antagonist) or hexamethonium did not. 4-AP increased TPVR, transiently in WKY but sustained in SHR. Yohimbine (α2-adrenoceptor antagonist) prevented the TPVR down-regulation in WKY. Reserpine and prazosin (α1-adrenoceptor antagonist) eliminated the late vasoconstriction in SHR. Plasma epinephrine overflow increased in nadolol-treated SHR. Through inhibition of KV, 4-AP activated parasympathetic ganglion transmission and peripheral, neuronal norepinephrine release. The sympathetic component dominated the 4-AP–HR-response in SHR. α2-adrenoceptor-dependent vasodilatation opposed norepinephrine-induced α1-adrenergic vasoconstriction in WKY, but not SHR. A βAR-activated, probably vagal afferent mechanism, hampered epinephrine secretion in SHR. Thus, 4-AP activated the autonomic system and exposed mechanisms relevant to hypertensive disease.

The Relationship between Menopausal Symptoms and Heart Rate Variability in Middle Aged Women

BackgroundThe study of the correlation of menopausal symptoms with heart rate variability (HRV) has not been adequate. The aim of this study was to investigate the relationship between postmenopausal symptoms measured by the menopause rating scale (MRS) and HRV.MethodsWe assessed postmenopausal symptoms (using MRS) with age, BMI, educational status, occupation, marital status, alcohol and caffeine consumption, smoking history, exercise, duration of sleep and amenorrhea, degree of anxiety and depression, menarcheal age, and heart rate variability. For evaluation of HRV, the record of electrocardiogram for 5 minutes in the resting state was divided into temporal categories and frequency categories, and analyzed.ResultsNo significant differences in age, BMI, duration of amenorrhea, heart rate, systolic blood pressure, diastolic blood pressure, fasting blood sugar, triglyceride, and high-density lipoprotein were observed between two groups, which were divided according to menopausal symptoms. Low frequency/high frequency (LF/HF) ratio was significantly higher in symptomatic women, compared with asymptomatic women (P < 0.05). No significant differences of HRV index by the severity of postmenopausal symptoms were observed. LF/HF ratio of HRV parameters showed a significant increase in moderate or severe degree of "hot flashes" and "sleep problem" score (P < 0.05). Anxiety scale in symptomatic women was significantly higher than in asymptomatic women (P < 0.05).ConclusionThe above data suggest that postmenopausal symptoms are associated with altered autonomic control of heart rate. In particular, hot flashes and sleep problems in moderate or severe degree are related to increase of sympathetic nerve activity.

Heart rate variability during motor and cognitive tasks in females with major depressive disorder

Research indicates that major depressive disorder (MDD) is associated with alterations in autonomic control, particularly cardiac control as measured by heart rate variability (HRV). In this preliminary study, we investigated the neural correlates of autonomic control by measuring both HRV and associated brain activity during the performance of mildly stressful tasks. Medically healthy female subjects with MDD ( N = 10) and healthy controls (N = 7) underwent H 2 15O-positron emission tomography (PET) and electrocardiographic ECG recording while performing a handgrip motor task and an n-back task. Indices of HRV were calculated and correlated with regional cerebral blood flow (rCBF). Differences in the rCBF and HRV correlations between depressed and healthy subjects were evident in both the medial and lateral orbital cortices. In addition, these areas appeared to be involved in different facets of autonomic control with regard to sympathetic or parasympathetic dominance of cardiac control. These results are consistent with the known roles of networks within the orbital cortex in both autonomic control and the pathophysiology of MDD.

Risk Assessment for Sudden Cardiac Death in Dialysis Patients

Patients with end-stage renal disease (ESRD) on long-term dialysis therapy have very high mortality due to predominantly cardiovascular causes1 (Figure 1). Sudden cardiac death (SCD) is the single most common form of death in dialysis patients, accounting for 20% to 30% of all deaths in this cohort.2,3 These patients indeed have a very high burden of coronary artery disease (CAD), and a proportion of SCD events could be due to obstructive CAD.1,2 However, epidemiological and observational studies have reported that the overall incidence of SCD in this population is much greater than the incidence of coronary events,4,5 and the risk of SCD persists even after coronary revascularization.6 These findings suggest a possibility of a primary increase in the risk of fatal ventricular arrhythmias, which is the most common cause of SCD. Dialysis patients with ESRD have several factors that could predispose them to a high risk of ventricular arrhythmias (Table 1). A large number of dialysis patients have diabetes, and thus, autonomic neuropathy as a consequence of both chronic uremia and coexisting diabetes is very common,7 resulting in alterations in autonomic control with a sustained increase in the sympathetic tone reported to be proarrhythmic. Similarly, hypertension is very common, and uremia leads to secondary hyperparathyroidism, both of which lead to considerable left ventricular hypertrophy (LVH).8 In addition, chronic uremia leads to endothelial dysfunction, and the combination of endothelial dysfunction and LVH compromises perfusion reserve and makes the individual susceptible to arrhythmias precipitated by ischemia. Long-standing uremia leads to uremic cardiomyopathy, with typical changes of diffuse myocardial fibrosis,9 which could lead to slowing of conduction and increased dispersion of repolarization, both of which have been shown to be proarrhythmic.10 Significant sudden shifts in electrolytes and fluid …

Impaired Decision Making in Oppositional Defiant Disorder Related to Altered Psychophysiological Responses to Reinforcement

When making decisions, children with oppositional defiant disorder (ODD) are thought to focus on reward and ignore penalty. This is suggested to be associated with a state of low psychophysiological arousal. This study investigates decision making in 18 children with oppositional defiant disorder and 24 typically developing control subjects. Children were required to choose between three alternatives that carried either frequent small rewards and occasional small penalties (advantageous), frequent large rewards and increasing penalties (seductive), or frequent small rewards and increasing penalties (disadvantageous). Penalties in the seductive and disadvantageous alternatives increased either in frequency or magnitude in two conditions. Heart rate (HR) and skin conductance responses to reinforcement were obtained. In the magnitude condition, children with ODD showed an increased preference for the seductive alternative (carrying large rewards); this was not observed in the frequency condition. Children with ODD, compared with typically developing children, displayed greater HR reactivity to reward (more HR deceleration) and smaller HR reactivity to penalty. Correlation analyses showed that decreased HR responses to penalty were related to an increased preference for large rewards. No group differences were observed in skin conductance responses to reward or penalty. The findings suggest that an increased preference for large rewards in children with ODD is related to a reduced cardiac reactivity to aversive stimuli. This confirms notions of impaired decision making and altered reinforcement sensitivity in children with ODD and adds to the literature linking altered autonomic control to antisocial behavior.

Association between vasomotor hot flashes and heart rate variability in recently postmenopausal women

The aim of this study was to investigate whether cardiovascular autonomic reactivity and risk profile are associated with the frequency and severity of hot flashes in recently postmenopausal women. A total of 150 postmenopausal women with varying degrees of severity of hot flashes (none, mild, moderate, or severe) underwent 24-hour electrocardiographic recording. The function of the autonomic nervous system was assessed via heart rate variability in time and frequency domains. The effects of hot flashes on cardiac autonomic function were studied by assessing heart rate variability in the presence and absence of symptoms. There were no differences in mean heart rate, heart rate extremes, or total number of ectopic beats between women without and women with mild, moderate, or severe hot flashes. However, most women (14/17, 82%) with frequent ventricular ectopic beats and all women with ventricular runs belonged to the symptomatic groups. Although there were no differences in 24-hour or nighttime heart rate variability between the study groups, the very-low-frequency spectral component of heart rate variability increased by 72% (P < 0.001) during the hot flash period compared with the control period and was accompanied by an increase in heart rate (3%; P < 0.001). Cardiovascular risk markers based on heart rate variability failed to show an association with the frequency and severity of hot flashes in recently postmenopausal women. However, during a hot flash episode, there were signs of altered autonomic control of heart rate, which may be involved in the regulatory mechanisms of hot flashes.

Impact of sleep on arrhythmogenesis.

Sleep is generally considered to be a protected period, when the cardiovascular system benefits from the restorative influences of the sleeping brain. However, the dynamics of cardiovascular control during sleep can tax the capacity of the diseased coronary circulation and myocardium with surges in sleep-state–related autonomic activity and disruptions in airway function and central nervous system regulation. In this regard, sleep may constitute an autonomic stress test for the heart. The scope of sleep-related risk for atrial and ventricular arrhythmias is substantial. The major subgroups susceptible to adverse influences of surges in autonomic activity during sleep are those with ischemic heart disease, heart failure, and channelopathies (Table).1 It is significant that 20% of myocardial infarctions and 15% of sudden deaths occur at night in the United States.2 Most atrial arrhythmias in patients younger than 61 years of age have nocturnal onset.3 The young are not immune to risk, as sudden infant death syndrome (SIDS) claims 2500 lives in the United States annually.4 Cardiovascular risk is compounded by comorbid factors, most notably apnea, which affects an estimated 4% to 9% of the general population5 and is considerably more prevalent among obese individuals.6 The more common form is obstructive sleep apnea (OSA), with partial or complete collapse of the pharynx. Half of heart failure patients experience either OSA or central sleep apnea (CSA) with central nervous system–mediated periodic breathing, commonly referred to as Cheyne-Stokes respiration. Such cardiorespiratory disturbances profoundly alter autonomic nervous system activity and increase risk of arrhythmia, hypertension, and myocardial infarction. View this table: Table. Patient Groups at Potentially Increased Risk for Nocturnal Cardiac Events It is surprising, as recently underscored by Malhotra and Loscalzo,7 that the significance of cardiovascular risk during sleep may not be duly recognized within the cardiology community. The reasons are …

Pulse transit time for scoring subcortical arousal in infants with obstructive sleep apnea

An altered autonomic control and response to respiratory events during sleep have been reported in infants with obstructive sleep apnea but appropriate methods are not established. We assessed the feasibility of pulse transit time (PTT) in detecting subcortical arousals in eight infants (median age 7 days) suffering from the Pierre Robin sequence and obstructive sleep apnea. Sleep studies including recordings of PTT performed before and after successful orthodontic treatment for their OSA were analyzed. PTT arousals (i.e., fall in PTT by > or =15 ms lasting for > or =3 s) were visually scored using specific analysis software. Apnea-related PTT arousals and spontaneous PTT arousals were distinguished and predicting factors for the occurrence of uninterpretable PTT signal and PTT arousals were analyzed. Six-hundred and seven apneas were analyzed. Uninterpretable PTT signal appeared in 394 (65%) apneas and were due to a disturbed pulse waveform in 63%. Predictors for the occurrence of uninterpretable PTT signal were type of apnea (odds ratio, 95% confidence interval for obstructive apnea = 0.5, 0.4-0.9) and duration of apnea (odds ratio, 95% confidence interval per second duration = 1.4, 1.3-1.5). Of 213 apneas with interpretable PTT signal, 43 (7% of all apneas) were followed by a PTT arousal. Predictor for their occurrence was treatment status (odds ratio, 95% confidence interval for pre-treatment status = 3.4, 1.3-8.8). Spontaneous PTT arousals during control periods appeared more frequently pre-treatment compared to post-treatment (41% vs. 16%; p-value = 0.001). There were only weak correlations between changes in PTT, heart rate, and arterial oxygen saturation (correlation coefficient <0.3). The feasibility of PTT in scoring apnea-related subcortical arousals in infants may be questionable. However, scoring spontaneous PTT arousals may be an approach for assessing sleep disruption in infants with obstructive sleep apnea.

Cardiac Mitochondrial Nitric Oxide: A Regulator of Heart Rate?

Alterations in autonomic control and myocardial nitric-oxide (NO) production are likely linked to the development and progression of heart dysfunction. By focusing on heart rate, the complexity of the actions of NO at distinct levels throughout the autonomic nervous system and its relationship with other regulators can be demonstrated. Given the multiple and opposing actions of NO on cardiac control, it is difficult to interpret a response after a global intervention in the NO system. The diversity of intracellular pathways activated by NO, and their differing sensitivities to different levels of NO, might account for some aspects of reported specific but opposite effects. We discuss factors that might contribute to this diversity of actions. A proper elucidation of the effects of NO on metabolic pathways and on energy generation could lead to novel therapeutic strategies aimed at the early treatment of heart dysfunction.

Effect of Slow Coronary Flow on P-Wave Duration and Dispersion

The slow coronary flow (SCF) phenomenon is often considered to be an incidental angiographic finding; however, several reports have shown it to be associated with cardiac events. In this study we aimed to assess P-wave duration and dispersion (PWD) in patients with SCF and to compare it with that of healthy subjects. Thus, 40 patients with angiographically proven SCF and otherwise normal coronary arteries (group 1) and 36 sex-age-matched healthy subjects (group 2) were included in this study. A 12-lead surface ECG, recorded at a paper speed of 50-mm/s and 2 mV/cm standardization, was obtained from each subject. P-wave duration was measured manually by use of a caliper. The difference between the maximum (Pmax) and minimum P (Pmin)-wave duration was calculated and defined as PWD. All subjects had undergone echocardiographic examination to exclude valvular disorders and wall motion abnormalities. There was no significant difference between the 2 groups in demographies of age, sex, heart rate, or blood pressure. Maximum P-wave duration and PWD were significantly higher in group 1 than in group 2 (120 +/-7 vs 115 +/-5, p = 0.003; 44 +/-12 vs 38 +/-9, p = 0.01, respectively). However, there was no significant difference in Pmin duration (75 +/-9 vs 78 +/-7, p = 0.4). In conclusion; SCF and otherwise normal epicardial coronary artery was found to be associated with prolonged P-wave duration and increased PWD. This may result from microvascular ischemia and/or altered autonomic control of cardiovascular system observed in this group of patients.

Changes in short-term measures of heart rate variability after eight weeks of cardiac rehabilitation

In coronary artery disease (CAD) and following myocardial infarction (MI), activity of the autonomic nervous system is altered. Reduced heart rate variability (HRV) is a risk factor for future cardiac event. Studies reporting changes in HRV post-cardiac rehabilitation (CR) are heterogeneous, due possibly to varied data collection and analysis protocols. To evaluate changes in spectral measures of HRV derived from 5-minute ECG recordings in patients completing an 8 weeks CR programme. Thirty-eight patients (21 males, 17 females, aged 65.6 +/- 11.6 years) underwent 5 minutes, supine ECG recordings and standard physiological and psychological assessment pre- and post-CR. A further 23 patients (14 males, 9 females aged 64.9 +/- 9 years) acted as controls. Outcome measures were: low frequency power, (LF, 0.04-0.15 Hz) high frequency power (HF, 0.15-0.40 Hz), LF:HF ratio and mean RR interval. Change was assessed by ANCOVA and paired t-tests. When compared with the CT group, the CR group showed significant increases in: SDNN (Delta +6 ms, CR vs. 0 ms CT), HFln (Delta 0.4 log units CR vs. 0 log units CT), LFln (Delta +0.6 log units CR, vs. +0.1 log units CT) and RR interval (Delta +30 ms, CR vs. -28 ms CT). This is the first study to show significant increases in raw LF and HF power derived from short-term ECG recordings in CR patients. These measures are risk factors for future cardiac event. As CR is associated with increases in these measures it may be viewed as an effective therapy capable of bringing about favourable alterations in autonomic control.

Intermittent hypobaric hypoxia exposure does not cause sustained alterations in autonomic control of blood pressure in young athletes

Intermittent hypoxia (IH), which refers to the discontinuous use of hypoxia to reproduce some key features of altitude acclimatization, is commonly used in athletes to improve their performance. However, variations of IH are also used as a model for sleep apnea, causing sustained sympathoexcitation and hypertension in animals and, thus, raising concerns over the safety of this model. We tested the hypothesis that chronic IH at rest alters autonomic control of arterial pressure in healthy trained individuals. Twenty-two young athletes (11 men and 11 women) were randomly assigned to hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normoxia (500 m) in a double-blind and placebo-controlled design. Both groups rested in a hypobaric chamber for 3 h/day, 5 days/wk for 4 wk. In the sitting position, resting hemodynamics, including heart rate (HR), blood pressure (BP), cardiac output (Q(c), C(2)H(2) rebreathing), stroke volume (SV = Q(c)/HR), and total peripheral resistance (TPR = mean BP/Q(c)), were measured, dynamic cardiovascular regulation was assessed by spectral and transfer function analysis of cardiovascular variability, and cardiac-vagal baroreflex function was evaluated by a Valsalva maneuver, twice before and 3 days after the last chamber exposure. We found no significant differences in HR, BP, Q(c), SV, TPR, cardiovascular variability, or cardiac-vagal baroreflex function between the groups at any time. These results suggest that exposure to intermittent hypobaric hypoxia for 4 wk does not cause sustained alterations in autonomic control of BP in young athletes. In contrast to animal studies, we found no secondary evidence for sustained physiologically significant sympathoexcitation in this model.

Effects of On-Road Highway Aerosol Exposures on Autonomic Responses in Aged, Spontaneously Hypertensive Rats

Epidemiological studies associate ambient particulate pollution with adverse health outcomes in elderly individuals with cardiopulmonary diseases. We hypothesized that freshly generated ultrafine particles (UFP) contribute to these effects, as they are present in high number concentrations on highways and vehicle passengers are exposed directly to them. Aged spontaneously hypertensive rats (9–12 mo) with implanted radiotelemetry devices were exposed to highway aerosol or filtered, gas-denuded (clean) air using an on-road exposure system to examine effects on heart rate (HR) and heart-rate variability (HRV). On the day of exposure, rats were pretreated with low-dose inhaled or injected lipopolysaccharide (LPS) to simulate respiratory tract or systemic inflammation, respectively. Exposures (6 h) in compartmentalized whole-body chambers were performed in an air conditioned compartment of a mobile laboratory on I-90 between Rochester and Buffalo, NY. HRV parameters were calculated from telemetric blood pressure signals and analyzed for the baseline period and for the first 32 h postexposure. The aerosol size (count median diameter = 15–20 nm; geometric standard deviation = 1.4–4.3) and number concentration (1.95–5.62 × 105/cm3) indicated the predominance of UFP. Intraperitoneal LPS significantly affected all of the parameters in a time-dependent manner; response patterns after inhaled or injected LPS pretreatment were similar, but more prolonged and greater in LPS-injected rats. A significant effect of highway aerosol was found, irrespective of pretreatment, which resulted in decreased HR in comparison to clean air-exposed rats. This effect was more persistent (∼ 14 h) in those rats that received ip LPS as compared to saline. The highway aerosol also significantly affected short-term alterations in autonomic control of HR, as evidenced by elevations in normalized high frequency power and decreased vagosympathetic balance. These findings show that environmental exposure concentrations of mixed traffic-related UFP/gas-phase emissions can affect the autonomic nervous system.

Complex autonomic dysfunction in cardiovascular, intensive care, and schizophrenic patients assessed by autonomic information flow

The cardiovascular control system is mediated by mechanisms acting at different time scales, such as heart period, vagal, sympathetic, and other slower controllers. Since these elements are interrelated in a complex manner, classical control theory fails and information-based description, based on autonomic information flow (AIF) functions, is appropriate. We investigated the hypothesis that AIF functions of typical time scales specifically characterize autonomic dysfunction and prognosis. Holter recordings of patients with multiple organ dysfunction syndrome (MODS) (26 survivors, 10 non-survivors), heart failure (13 low risk, 13 high risk of cardiac arrest), idiopathic dilated cardiomyopathy (IDC) (26 low risk, 11 high risk), after abdominal aorta surgery (AAS) [32 with length of stay in hospital (LOS) >7 days; 62 with LOS < or =7 days] or with schizophrenia (n=20) were assessed and compared to 20 control subjects. We found different AIF time scales discriminating risk. AIF measures of heart beat period had predominant prognostic value in heart failure patients, those of vagal communication in MODS and IDC, and those of long-term communication after AAS. Schizophrenic patients were discriminated from controls by vagally mediated communication. Different time scales of AIF represent specific pathophysiological aspects of altered complex autonomic control (communication) and consequently have predictive implications.

The use of heart rate variability measures to assess autonomic control during exercise

Heart rate variability (HRV) is a non-invasive indicator of cardiac autonomic modulation at rest. During rhythmic exercise, global HRV decreases as a function of exercise intensity. Measures reflecting sympathovagal interactions at rest do not behave as expected during exercise. This makes interpretation of HRV measures difficult, especially at higher exercise intensities. This problem is further confounded by the occurrence of non-neural oscillations in the high-frequency band due to increased respiratory effort. Alternative data treatments, such as coarse graining spectral analysis (CGSA), have demonstrated expected changes in autonomic function during exercise with some success. The separation of harmonic from fractal and/or chaotic components of HRV and study of the latter during exercise have provided further insight into cardioregulatory control. However, more research is needed. Some cross-sectional differences between HRV in athletes and controls during exercise are evident and data suggest longitudinal changes may be possible. Standard spectral HRV analysis should not be applied to exercise conditions. The use of CGSA and non-linear analyses show much promise in this area. Until further validation of these measures is carried out and clarification of the physiological meaning of such measures occurs, HRV data regarding altered autonomic control during exercise should be treated with caution.

Low Plasma Volume Coincides With Sympathetic Hyperactivity and Reduced Baroreflex Sensitivity In Formerly Preeclamptic Patients

Preeclampsia is associated with enhanced sympathetic activity as well as subnormal plasma volume. Meanwhile, in over 50% of these complicated pregnancies, the subnormal plasma volume has been found to persist for a prolonged period after pregnancy. The objective of this study is to test the hypothesis that in normotensive formerly-preeclamptic women, persistence of a subnormal plasma volume coincides with enhanced sympathetic activity and with it, an altered autonomic control of blood pressure. Forty-eight formerly-preeclamptic women participated in this study. After measurement of their plasma volume by iodine 125-albumin indicator dilution, they were subdivided into a group with a normal plasma volume (plasma volume > 48 ml/kg lean body mass) and a group with a subnormal plasma volume (< or = 48 ml/kg lean body mass). We performed spectral analysis on their beat-to-beat blood pressure and heart rate recordings and compared both groups using non-parametric tests. Formerly-preeclamptic women with a subnormal plasma volume had a higher sympathetic activity (P = .001) and a lower baroreflex sensitivity (P = .04) than their counterparts with a normal plasma volume. In normotensive formerly-preeclamptic women, a subnormal plasma volume coincides with a higher sympathetic activity in the blood pressure regulation and lower baroreflex sensitivity. Whether these alterations in the autonomic control mechanisms are a cause or effect of the subnormal plasma volume remains to be elucidated.