H.G. van Steenis

Characterization of stress reactions to the stroop color word test

Sympatho-adrenal activation induced by stress contributes to the development of pathological states such as hypertension and anxiety disorders. The Stroop Color Word Test (CWT) is evaluated as a test for the study of stress-induced sympathetic effects, on the basis of psychological, physiological and biochemical responses. The CWT induced increases in plasma and urinary adrenaline, heart rate, respiration rate, electrodermal activity, electromyography, feelings of anxiety, and decreased finger pulse amplitude.

Heart rate variability spectra based on non-equidistant sampling: the spectrum of counts and the instantaneous heart rate spectrum

This paper compares two methods to estimate heart rate variability spectra, i.e., the spectrum of counts and the instantaneous heart rate spectrum. Contrary to Fourier techniques based on equidistant sampling of the interbeat intervals, the spectrum of counts and the instantaneous heart rate spectrum are based on non-equidistant sampling: the values are determined at R-wave moments. A consequence of the non-equidistant occurrence of the R-peaks in a heart rate signal is the appearance of the sidebands of the harmonic components of the mean heart rate in the spectra. These sidebands contaminate the signal components in the spectrum. The sideband distortion in the instantaneous heart rate spectrum was found to be smaller than in the spectrum of counts. Simulations using the IPFM-model were made to quantify this difference. On the basis of these simulations, sideband distortion appeared to be dependent on the mean heart rate, the modulation depth and the modulation frequency.

EFFECTS OF LORAZEPAM ON CARDIAC VAGAL TONE DURING REST AND MENTAL STRESS - ASSESSMENT BY MEANS OF SPECTRAL-ANALYSIS

Dose-dependent effects of intravenously administered lorazepam on haemodynamic fluctuations were studied by means of spectral analysis, in order to elucidate sympathetic and parasympathetic components in cardiovascular control during situations of rest and mental stress after benzodiazepine administration. In a double-blind randomized cross-over study, nine male volunteers participated in two sessions: a placebo and lorazepam session. During these sessions, the subjects repeatedly performed a 10-min version of the Stroop Color Word Test (CWT), with 10 min of rest between the CWTs. Lorazepam was administered before each rest period in increasing doses of 0.0, 0.06, 0.13, 0.25 and 0.5 mg (total cumulative dose: 0.94 mg). During the placebo session the subjects received five placebo injections. For five of the nine subjects the lorazepam session was their first session. Heat rate (HR), blood pressure (BP) and respiration were recorded continuously. Power spectra were calculated per 2.5-min periods for HR, systolic (SBP) and diastolic BP (DBP). Spectral density was assessed for three frequency bands: low (LFB: 0.02–0.06 Hz), mid (MFB: 0.07–0.14 Hz) and high (HFB: 0.15–0.40 Hz). During the consecutive periods of rest, lorazepam induced a dose-dependent decrease in HR, and a dose-dependent increase in LFB, MFB and HFB power of HR, but lorazepam had no effect on BP. The effects were significant after 0.44 mg lorazepam for HR and HFB power, and after 0.94 mg lorazepam for the HR fluctuations in the LFB and MFB. Lorazepam did not influence the cardiovascular responses to the CWT. Our data underline that benzodiazepines can exert a specific influence on parasympathetic activity: lorazepam induced dose-dependent increases in cardiac vagal tone, resulting in decreased HR and increased HR variability, but only during periods of rest. The increase in vagal tone observed after low doses of lorazepam was not related to diminished sympathetic activity, altered respiration, or increased sedation.

Cardiovascular variability after clonidine challenge: assessment of dose-dependent temporal effects by means of spectral analysis.

Effects of four intravenous (i.v.) doses (0.25, 0.5, 1, and 2 μg/kg) of the α2-adrenoceptor agonist clonidine (CLO) were studied in 7 normotensive male volunteers in a placebo-controlled double-blind randomized design to evaluate the role of α2-adrenoceptors in spontaneous short-term cardiovascular fluctuations. Heart rate (HR), systolic and diastolic blood pressure (SBP, DBP; Finapres device), stroke volume (SV) and total peripheral resistance (TPR) were monitored for 1 h after infusion of CLO while the subjects rested in a semirecumbent position. For HR, SBP, and DBP, power spectra and variation coefficients were calculated for consecutive time segments of 2.5 min. Power density was assessed for three frequency bands: low (LFB, 0.02–0.06 Hz), mid (MFB, 0.07–0.14 Hz), and high (HFB, 0.15–0.40 Hz). Per time-segment, baroreflex sensitivity (BRS) was estimated as the gain (or modulus) in MFB between systolic pressure values and R-R interval times. Decreases in mean levels of SBP and DBP were observed within 15 min after infusion of ≥0.5 μg/kg CLO. HR first showed a slight increase 15 min after infusion of 0.5, 1, and 2 μg/kg CLO, but decreased subsequently as in all doses, including placebo. SV and TPR decreased after a dose of 2 μg/kg CLO. LFB and MFB power of HR were reduced after 2 μg/kg CLO, but only during the first 30 min after infusion; during this period, respiratory depth was also diminished, indicating that these effects may reflect a reduction in sympathetic outflow as well as a reduction in vagal outflow. Respiratory frequency did not change after CLO, nor did BRS. DBP MFB power was reduced after 2 μg/kg CLO during the entire postinfusion period, probably as a reflection of reduced sympathetic outflow. SBP HFB power was significantly increased after ≥0.5 μg/kg CLO, but only after 30 min of infusion, which could be a consequence of alterations in both vagal outflow and mechanical respiratory properties. Thus, in a dose range of 0.25–2 μg/kg CLO, significant effects were detected for SBP, DBP, and HR after ≥0.5 μg/kg, whereas spontaneous short-term fluctuations of HR and DBP were influenced only after a dose of 2 μg/kg. The effects were slight but could be detected within a postinfusion period of 1 h. Our data show that sequential spectral analysis of spontaneous hemodynamic fluctuations can be used to unravel time-dependent dynamics of sympathetic and vagal components in short-term cardiovascular control.

Cardiovascular, Neuroendocrine, and Sedative Responses to Four Graded Doses of Clonidine in a Placebo-Controlled Study

Effects of four doses of the alpha 2-receptor agonist clonidine (CLO) (0.25, 0.5, 1, and 2 micrograms/kg IV) and placebo were studied in seven healthy men who volunteered in a double-blind randomized design in order to delineate possible presynaptic and postsynaptic components in the mechanism of action of CLO. Blood pressure, heart rate, plasma noradrenaline (NOR), plasma 3-methoxy-4-hydroxyphenylglycol (MHPG), plasma growth hormone (GH), and subjective sedation were monitored for a period of 1 hr following infusion of CLO. NOR and MHPG were also analyzed in urine, collected at 1 and 4 hr after the infusions. Dose-dependent decrements were observed in systolic and diastolic blood pressure and plasma NOR levels, and dose-dependent increases in subjective sedation and plasma GH. CLO did not influence plasma MHPG levels, whereas only urinary MHPG excretion was reduced 4 hr after infusion of 2 micrograms/kg CLO. Because no obvious differences between dose-response relations of plasma NOR (believed to be a presynaptic and peripheral effect), blood pressure (believed to be mainly a central presynaptic and postsynaptic effect), and subjective sedation (believed to be a central and probably postsynaptic effect) were observed, our results do not provide simple parameters to discern the multiple mechanisms of action of CLO. However, at a dose of 0.5 micrograms/kg CLO (a dose lower than that generally used) clear effects on plasma NOR, blood pressure, and sedation, but not on plasma GH (a central postsynaptic effect) or urinary MHPG (a presynaptic effect), were observed. When using CLO as a challenge test in psychiatric disorders, a design with 0.5 micrograms/kg CLO, in addition to the traditional 2 micrograms/kg CLO, may provide more information to characterize discrete abnormalities in the noradrenergic system at the level of the brainstem, the pituitary, or the peripheral sympathetic nervous system.

Sleep patterns and blood pressure variability in patients with pure autonomic failure

Sleep patterns and 24-h blood pressure variability were studied in four female patients (age range: 56–82 years) with pure autonomic failure. All patients had severe symptomatic postural hypotension, without neurological deficits. In these patients the following patterns were observed: (i) a reversed diurnal blood pressure pattern, with the highest values observed at sleep onset; (ii) a prolonged sleep latency and increased amount of stage 3 sleep; (iii) difficulty with getting up after awakening in the morning, due to severe postural hypotension; (iv) an absence of prominent respiratory abnormalities during sleep; and (v) a dissociation between respiratory and haemodynamic findings. It is concluded that isolated deficiency of presumed postganglionic autonomic function influences sleep architecture, probably through absence of buffering of diurnal haemodynamic alterations, such as by postural hypotension and its consequences for body fluid volume regulation. This may be of relevance when sleep patterns are studied in other types of autonomic failure with postural hypotension involving central or preganglionic lesions, as in patients with the Shy—Drager syndrome or multiple system atrophy.Sleep patterns and 24-h blood pressure variability were studied in four female patients (age range: 56–82 years) with pure autonomic failure. All patients had severe symptomatic postural hypotension, without neurological deficits. In these patients the following patterns were observed: (i) a reversed diurnal blood pressure pattern, with the highest values observed at sleep onset; (ii) a prolonged sleep latency and increased amount of stage 3 sleep; (iii) difficulty with getting up after awakening in the morning, due to severe postural hypotension; (iv) an absence of prominent respiratory abnormalities during sleep; and (v) a dissociation between respiratory and haemodynamic findings. It is concluded that isolated deficiency of presumed postganglionic autonomic function influences sleep architecture, probably through absence of buffering of diurnal haemodynamic alterations, such as by postural hypotension and its consequences for body fluid volume regulation. This may be of relevance when sleep patterns are studied in other types of autonomic failure with postural hypotension involving central or preganglionic lesions, as in patients with the Shy—Drager syndrome or multiple system atrophy.

Psychological, cardiovascular, and endocrine changes during 6 hours of continuous infusion of epinephrine or norepinephrine in healthy volunteers.

&NA; Psychological, cardiovascular, endocrine, and metabolic reactions to a sustained infusion of epinephrine (E) and norepinephrine (NE) were studied in 10 healthy male volunteers in a placebo‐controlled randomized design. The subjects participated each in three sessions during which they received 6‐hr infusion of either E (82 pmol/kg/min), NE (178 pmol/kg/min), or placebo (PLA) (saline, 5.4 ml/hr). Heart rate and intra‐arterial blood pressure were recorded continuously. Blood samples for assay of catecholamines, cortisol, prolactin, growth hormone, insulin, triglycerides, and glucose were obtained at regular intervals. Changes in subjective mood were assessed with the Profile of Mood States (POMS) and the State‐Trait Anxiety Inventory (STAI). During infusion of E, arterial plasma epinephrine levels increased 10‐fold, which induced significant increases in heart rate, plasma insulin, and glucose levels, and decreases in mean arterial pressure (MAP) and diastolic pressure (DAP). NE infusion caused a 5‐fold arterial plasma norepinephrine increase and induced a significant decrease in heart rate and increases in MAP, DAP, and glucose levels. The effects were present shortly after initiation of the infusions, remained fairly constant during the 6‐hr infusion period and disappeared within 1 hr after the infusions had been stopped. Changes in subjective mood were not observed during the infusions, nor after the infusions had been stopped. Infusion of E or NE also had no significant effect on systolic blood pressure, plasma prolactin, growth hormone, cortisol, and triglycerides. Our results show that moderate cardiovascular and metabolic effects can be caused by sustained increases in circulating catecholamines.(ABSTRACT TRUNCATED AT 250 WORDS)

A Comparison Of Two Methods To Calculate The Heart Rate Spectrum Based On Non-equidistant Sampling

Time-dependent beat-to-beat fluctuations in cardiovascular parameters can be studied by means of spectral analyses based on a nonequidistant sampling of the signals [1,2]. This method has been used to study variability in inter-beat interval length and systolic blood pressure. The present study compares two methods to calculate heart rate spectra, based on the principle of non-equidistant sampling.

The instantaneous frequency of cardiovascular time series: a comparison of methods

The instantaneous frequency (IF) of cardiovascular time series is used to describe the time-varying spectral contents of the characteristic frequency bands that are of interest for psychophysiological and cardiovascular research. Four methods to compute IF of band-limited, monocomponent, and analytical cardiovascular time series were compared by means of simulated time series contaminated with additive noise. These four methods are: the method using the inverse Fourier transform of uncorrelated time-slices of the Wigner-Ville distribution, the discrete time-frequency transform, the circular mean direction of the time-slices of the Wigner-Ville distribution, and the central finite difference of the phase. The time resolution of the estimates is optimal and is inversely related to the bandwidth of the frequency components, as given by the uncertainty principle of Gabor. At periods in time where the signal fulfills the requirements of the model signal, the four estimates of IF are numerically equal; only the circular mean direction showed a slight deviation from the other estimates. Although the estimates of IF differ at sudden phase shifts at low amplitude, i.e. at points where the signal locally does not comply with the requirements of the model signal, overall the four methods produce comparable estimates of IF of a cardiovascular time series at an optimal time resolution.

A new method to estimate the instantaneous frequency and bandwidth of cardiovascular time series

Describes a new method to quantify the time-varying spectral content of non-stationary cardiovascular time series by means of the instantaneous amplitude, frequency, and bandwidth. Though the described method is computational complex, it produces better estimates of the IF and, in particular, the LB than other algorithms using time-frequency distributions or direct methods (i.e. differentiating the phase of the analytical time series). In contrast to sequential spectral analysis of short time windows, the method presented may provide instantaneous information on the time-dependent changes in sympathetic and parasympathetic activity within the cardiovascular control system (CCS).