Effects of age and gender on autonomic control of blood pressure dynamics.
(17/2230)
Both age and gender influence cardiovascular autonomic control, which in turn may influence the ability to withstand adverse cardiac events and respond to orthostatic stress. The purpose of this study was (1) to quantify age- and gender- related alterations in autonomic control of blood pressure (BP) and (2) to examine the impact of these autonomic alterations on BP response to orthostatic stress. We measured continuous BP and R-R intervals and vasoactive peptide levels in the supine and 60 degrees head-up tilt positions during paced respiration (0.25 Hz) in 89 carefully screened healthy subjects (41 men, 48 women, aged 20 to 83 years). Data were analyzed by gender (age adjusted) and by age group (gender adjusted). During tilt, women had greater decreases in systolic BP than men (-10.2+/-2 versus -1.2+/-3 mm Hg; P=0.02) and smaller increases in low-frequency (sympathetically mediated) BP power (P=0.02). Upright plasma norepinephrine was lower in women (P=0.02). Women had greater supine high-frequency R-R interval power than men (P=0.0001). In elderly subjects, the tilt-induced increase in low-frequency BP power was also diminished (P=0.01), despite higher supine (P=0.02) and similar upright norepinephrine levels compared with younger subjects. Thus, healthy women have less sympathetic influence on BP and greater parasympathetic influence on R-R interval than men. Elderly subjects also have reduced sympathetic influence on BP, but this appears to be more consistent with a reduction in vasomotor sympathetic responsiveness. (+info)
Power spectral analysis of heart rate variability during hyperinsulinemia in nondiabetic offspring of type 2 diabetic patients: evidence for possible early autonomic dysfunction in insulin-resistant subjects.
(18/2230)
Sympathetic activation has been considered as a link between insulin resistance, hyperinsulinemia, and hypertension. However, little is known about the association between insulin sensitivity and autonomic regulation or about the effect of acute hyperinsulinemia on cardiac sympathovagal balance. The aim of this study was to investigate heart rate variability (HRV) during the euglycemic-hyperinsulinemic clamp in nondiabetic offspring of patients with type 2 diabetes. We studied 35 nondiabetic offspring of patients with type 2 diabetes and 19 control subjects. Probands were chosen from a 10-year follow-up study of patients with well-characterized type 2 diabetes according to their fasting C-peptide level (selected from both ends of the distribution) and from control subjects to form three groups: 1) a group including subjects who were offspring of type 2 diabetic patients with low C-peptide levels (deficient insulin secretion group [IS group], n = 17), 2) a group including subjects who were offspring of type 2 diabetic patients with high C-peptide levels (insulin-resistant group [IR group], n = 18), and 3) a control group without a history of type 2 diabetes in first-degree relatives (n = 19). HRV was assessed at baseline and at the steady state during the euglycemic-hyperinsulinemic clamp. Rates of whole-body glucose uptake (M value) were lower in the IR group than in the IS group and the control group (41+/-3 vs. 54+/-2 vs. 60+/-4 micromol x kg(-1) x min(-1), P < 0.01 and P < 0.01, respectively). In all groups, heart rate increased significantly during hyperinsulinemia. In the IR group, insulin infusion increased total power of HRV [from 7.70+/-0.15 to 8.05+/-0.15 ln(ms2), P < 0.01] and the low frequency-to-high frequency ratio (from 0.62+/-0.14 to 1.14+/-0.18, P < 0.01) and decreased power of the high frequency spectral component (from 5.73+/-0.17 to 5.43+/-0.16 ln(ms2), P < 0.05), whereas in other groups, changes in HRV were not significant. We conclude that the HRV response to acute hyperinsulinemia in the offspring of type 2 diabetic probands was likely to be modulated by the type 2 diabetic phenotype of the parent. In insulin-resistant subjects, autonomic dysfunction may be an earlier defect than hitherto acknowledged. (+info)
Neurally mediated cardiac syncope: autonomic modulation after normal saline infusion.
(19/2230)
OBJECTIVES: This study assessed the heart variability response to orthostatic stress during tilt table testing before and after normal saline administration. BACKGROUND: The efficacy of sodium chloride and mineralocortoid in the treatment of neurally mediated cardiac syncope is attributed to intravascular volume expansion; however, their modulation of autonomic nervous system activity has not been evaluated. METHODS: Heart rate variability analysis was performed on 12 adolescents with a history of syncope or presyncope (mean age 15.2+/-0.7 years) during tilt table testing. Subjects were upright 80 degrees for 30 min or until syncope. After normal saline administration, the patient was returned upright for 30 min. Heart rate variability analysis data were analyzed by an autoregression model (Burg method). RESULTS: All subjects reproducibly developed syncope during control tilt table testing; median time to syncope was 9.4+/-2.1 min. After normal saline infusion, none of the subjects developed syncope after 30 min upright. In the control tilt, there was an initial increase followed by a progressive decrease in low frequency power until syncope. Repeat tilt after normal saline administration demonstrates that low frequency power increased but the magnitude of initial change was blunted when compared with control. In addition, low frequency power increased during normal saline tilt sequence compared with the control tilt, during which it decreased. CONCLUSIONS: Normal saline blunted low frequency power stimulation and prevented paradoxical low frequency power (sympathetic) withdrawal. Increasing intravascular volume with normal saline alters autonomic responses that may trigger neurally mediated syncope reflexes. (+info)
Role of nitric oxide in the regulation of cardiovascular autonomic control.
(20/2230)
Alteration in function of the cardiac autonomic nervous system has proved to be a powerful predictor of cardiac death or serious arrhythmia in patients with cardiac disease, yet little is known about the mechanisms by which this system is regulated. Recent evidence suggests that the gaseous molecule nitric oxide (NO) may act as an important mediator in this pathway. Histochemical staining techniques have identified neuronal populations that contain NO synthase within medullary cardio-regulatory sites and their peripheral autonomic pathways. Drugs that modulate the NO pathway (administered both systemically and into the central nervous system) cause changes in pre- and post-ganglionic sympathetic nerve activity that imply that NO serves to inhibit central sympathetic outflow. There is also evidence that NO may attenuate cardiovascular end-organ responses to sympathetic stimulation. Studies suggest that NO modulates cardiac vagal control, increasing the activity of central vagal motoneurons and, more contentiously, contributing to the bradycardic effects of vagal stimulation. NO also modulates so-called 'indirect' vagal inhibition of sympathetic cardiac responses. Additionally, central attenuation of baroreflex-mediated vagal control has been described. There is relatively little information available on the importance of NO in the regulation of human cardiovascular autonomic control. Further well-controlled studies are required. (+info)
Alterations of autonomic nervous activity in recurrence of variant angina.
(21/2230)
OBJECTIVE: To investigate whether autonomic nervous activity is involved in the recurrence of spontaneous coronary spasm in variant angina. DESIGN: Retrospective analysis. SETTING: Cardiology department of a university hospital. PATIENTS: 18 patients with variant angina were divided into single attack group (SA; nine patients) and multiple attack group (MA; nine patients) according to the frequency of ischaemic episodes with ST segment elevation during 24 hour Holter monitoring. METHODS: Heart rate variability indices were calculated using MemCalc method, which is a combination of the maximum entropy method for spectral analysis and the non-linear least squares method for fitting analysis, at 30 second intervals for 30 second periods, from 40 minutes before the attack to 30 minutes after the attack. High frequency (HF; 0.04-0.15 Hz) was defined as a marker of parasympathetic activity, and the ratio of low frequency (LF; 0.15-0.40 Hz) to high frequency (LF/HF) as an indicator of sympathetic activity. The averaged value during the 40 to 30 minute period before an attack was defined as the baseline. RESULTS: Compared with baseline, the HF component decreased in both groups at two minutes before the attack (p < 0.01), and the LF/HF ratio decreased at three minutes before the attack (p < 0.01). The baseline LF/HF was lower in the MA group than in the SA group (p < 0. 01). CONCLUSIONS: A reduction of sympathetic activity may play a key role in determining the recurrence of transient ischaemic events caused by spontaneous coronary spasm in patients with variant angina. (+info)
Daily variation of particulate air pollution and poor cardiac autonomic control in the elderly.
(22/2230)
examined the cardiac autonomic response to daily variations in PM in 26 elderly (mean age 81) individuals for 3 consecutive weeks. Several standardized methods were used to measure 24-hr average PM concentrations prior to the clinical test inside (indoor PM2.5) and immediately outside (outdoor PM2.5 and PM2.5-10) of participants' residences. Resting, supine, 6-min R wave to R wave (R-R) interval data were collected to estimate high frequency (0.15-0.40 Hz) and low frequency (0.04-0.15 Hz) powers and standard deviation of normal R-R intervals (SDNN) as cardiac autonomic control indices. Participant-specific lower heart rate variability days were defined as days for which the high-frequency indices fell below the first tertile of the individual's high-frequency distribution over the study period. Indoor PM2.5 > 15 microg/m3 was used to define high pollution days. Results show that the odds ratio (95% confidence interval) of low heart rate variability high frequency for high (vs. not high) pollution days was 3.08 (1.43, 6.59). The ss-coefficients (standard error) from mixed models to assess the quantitative relationship between variations in indoor PM2.5 and the log-transformed high frequency, low frequency, and SDNN were: -0.029 (0.010), -0.027 (0.009), and -0.004 (0.003), respectively. This first study of cardiac autonomic control response to daily variations of PM2.5 indicates that increased levels of PM2.5 are associated with lower cardiac autonomic control, suggesting a possible mechanistic link between PM and cardiovascular disease mortality. (+info)
Neuroendocrine and psychophysiologic responses in PTSD: a symptom provocation study.
(23/2230)
Biological research on post-traumatic stress disorder (PTSD) has focused on autonomic, sympatho-adrenal, and hypothalamo-pituitary-adrenal (HPA) axis systems. Interactions among these response modalities have not been well studied and may be illuminating. We examined subjective, autonomic, adrenergic, and HPA axis responses in a trauma-cue paradigm and explored the hypothesis that the ability of linked stress-response systems to mount integrated responses to environmental threat would produce strong correlations across systems. Seventeen veterans with PTSD, 11 veteran controls without PTSD, and 14 nonveteran controls were exposed to white noise and combat sounds on separate days. Subjective distress, heart rate, skin conductance, plasma catecholamines, ACTH, and cortisol, at baseline and in response to the auditory stimuli, were analyzed for group differences and for patterns of interrelationships. PTSD patients exhibited higher skin conductance, heart rate, plasma cortisol, and catecholamines at baseline, and exaggerated responses to combat sounds in skin conductance, heart rate, plasma epinephrine, and norepinephrine, but not ACTH. The control groups did not differ on any measure. In canonical correlation analyses, no significant correlations were found between response systems. Thus, PTSD patients showed heightened responsivity to trauma-related cues in some, but not all, response modalities. The data did not support the integrated, multisystem stress response in PTSD that had been hypothesized. Individual response differences or differing pathophysiological processes may determine which neurobiological system is affected in any given patient. (+info)
Activation of outward K+ currents: effect of VIP in oesophagus.
(24/2230)
1. Electrical field stimulations (EFS) of the opossum and canine lower oesophageal sphincters (OLOS and CLOS respectively) and opossum oesophageal body circular muscle (OOBCM) induce non-adrenergic, non-cholinergic (NANC) relaxations of any active tension and NO-mediated hyperpolarization. VIP relaxes the OLOS and CLOS and any tone in OOBCM without major electrophysiological effects. These relaxations are not blocked by NOS inhibitors. Using isolated smooth muscle cells, we tested whether VIP acted through myogenic NO production. 2. Outward currents were similar in OOBCM and OLOS and NO increased them regardless of pipette Ca2+(i), from 50-8000 nM. L-NAME or L-NOARG did not block outward currents in OLOS at 200 nM pipette Ca2+. 3. Outward currents in CLOS cells decreased at 200 nM pipette Ca2+ or less but NO donors still increased them. VIP had no effect on outward currents in cells from OOBCM, OLOS or CLOS under conditions of pipette Ca2+ at which NO donors increased outward K+ currents. 4. We conclude, VIP does not mimic electrophysiological effects of NO donors on isolated cells of OOBCM, OLOS or CLOS. VIP relaxes the OLOS and CLOS and inhibits contraction of OOBCM by a mechanism unrelated to release of myogenic NO or an increase in outward current. 5. Also, the different dependence of outward currents of OOBCM and OLOS on pipette Ca2+ from those of CLOS suggests that different K+ channels are involved and that myogenic NO production contributes to K+ channel activity in CLOS but not in OLOS or OOBCM. (+info)