Decrease In Total Power Research Articles

Heart rate variability during the first 24 hours of successfully reperfused acute myocardial infarction: Paradoxic decrease after reperfusion

Heart rate variability (HRV) was evaluated during the first 24 hours of hospitalization in 36 patients with acute myocardial infarction. Reperfusion was achieved by 60 minutes in 21 patients (group M1) and by 130 minutes in the remaining 15 (group M2). Mean 24-hour HRV measures were not significantly different between groups M1 and M2. Hourly spectral analysis revealed a decrease in total power (0.01 to 1.0 Hz) from 0 to 8 hours to 9 to 16 and 17 to 24 hours in groups M1 (7.04 ± 0.27 to 6.94 ± 0.23 and 6.52 ± 0.18; p = 0.0006) and in group M2 (6.88 ± 0.30 to 6.57 ± 0.23 and 6.40 ± 0.15; p = 0.002). Total power decreased immediately after reperfusion: in group M1 it decreased during the second hour (7.32 ± 0.96 to 6.42 ± 1.2; p = 0.001) and in group M2 during the third (7.47 ± 1.2 to 6.73 ± 1.4; p = 0.049) and fourth hours (7.47 ± 1.2 to 6.48 ± 1.4; p = 0.029). Mean change in total power in the second hour was −11.8% in group M1 and +3.9% in group M2 ( p = 0.0001) and in the third hour, +14.5% in group M1 and −8.6% in group M2 ( p = 0.006). During the remaining 21 hours, there was no significant difference in hourly change in total power between groups. Similar changes were noted in high-frequency power, but the ratio of low-frequency to high-frequency power was unchanged. In acute myocardial infarction, HRV is higher during the early phase and decreases as hours progress. Reperfusion causes an immediate, transient, and seemingly paradoxic decrease in HRV, probably because of an abrupt decrease in parasympathetic tone.

Vibroacoustic stimulation with a complex signal: effect on behavioral state in fetal sheep.

An ideal vibroacoustic stimulus for testing fetal reactivity has yet to be developed. In the present study in fetal sheep we tested the effect on behavioral state of an amplitude and frequency-modulated signal produced at the abdominal surface of the ewe. The stimulus was presented during periods of fetal non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. Evaluation of behavioral state was accomplished by visual observation of strip-chart recordings. Assessed in this manner, vibroacoustic stimulation during NREM sleep consistently resulted in a change to an indeterminate state. However, stimulation during REM sleep failed to have an effect. Additional evaluation applying spectral analysis to the fetal electrocorticogram during stimulation in NREM sleep revealed a marked decrease in delta band power from 100 to 27 +/- 5% and in theta band power from 100 to 40 +/- 4% resulting in a decrease in total power from 100 to 35 +/- 4% (p < 0.05). Stimulation during REM sleep revealed a significant increase in beta band power from 100 to 123 +/- 14%. Vibroacoustic stimulation in both NREM and REM sleep led to an increase in spectral edge frequency, implying central arousal.

Pure autonomic failure: Complex abnormalities in the neural mechanisms regulating the cardiovascular system

The aim of this study was to evaluate the sympatho-vagal interaction modulating cardiovascular function and the possible impairment of baroreceptor sensitivity in patients affected by Pure Autonomic Failure (PAF). We studied 4 patients affected by PAF and 7 controls at rest and during different levels (45°, 60°, 90°) of head-up tilt. On a different day all subjects underwent i.v. administration of phenylephrine at dosages adequate to enhance systolic blood pressure by about 20 mmHg both at rest and during 45° head-up tilt. Finally, 1.5 mg atropine was infused intravenously only in the patients. Spectral analysis of RR interval and systolic arterial pressure (SAP) variabilities provided markers of sympathetic (low-frequency oscillations, about 0.1 Hz, LF RR) and vagal (high-frequency oscillations, about 0.25 Hz, HF RR) modulations of heart period and of sympathetic vasomotor activity (low-frequency oscillations of SAP variability, LF SAP). Baroreceptor mechanisms were quantified by means of the index α (calculated from the square root of the ratio between the powers of HF components of RR interval and SAP variabilities) and of the phenylephrine RR-SAP slope. Patients affected by PAF were characterized by a drastic decrease in total power of RR variability and by the absence of LF RR and LF SAP components. Moreover, HF RR, although largely predominant in its relative value, was also markedly reduced in its absolute value. Finally, the baroreceptive mechanisms appeared to be heavily impaired. In conclusion, PAF patients seem to be characterized by a complex alteration of neural mechanisms, which in addition to the signs of a sympathetic denervation include an impairment, at least functional, of the vagal modulation of heart rate.

Topographic pharmaco‐EEG mapping of increasing doses of buspirone and its comparison with diazepam

AbstractIt has been argued that representative drugs of the main psychopharmacological classes induce similar pharmaco‐EEG changes within groups but different changes between groups. The aim of this double‐blind, cross‐over, placebocontrolled study was to evaluate the effects of single oral doses of buspirone (BUS) 5, 15 and 30 mg in 15 healthy young subjects of both sexes on topographic maps of quantiative pharmaco‐EEG, using diazepam (DZP) 10 mg as reference compound. Sixteen lead recordings of three‐minute vigilance‐controlled EEG (V‐EEG) and four‐minute resting EEG (R‐EEG) were assessed at 0, 1, 2, 4, 6 and 8 hours after drug intake. EOG activity (vertical and horizontal) was also recorded in order to minimize ocular artifacts before applying an automatic artifact rejection method. MANOVA/Hotelling T2 maps (multivariate analysis) showed a highly significant differentiation of DZP from placebo from the 1 st until the 8th hour all over the brain. After BUS a clear dose‐response was observed with effects being greater and longer lasting with increasing doses, the highest showing a peak effect in the 2nd hour which lasted until the 4th hour, mostly in central regions. Maps of drug‐induced pharmaco‐EEG changes as compared to placebo‐induced alterations (univariate analysis) demonstrated typical ‘anxiolytic pharmaco‐EEG patterns’ after DZP, characterized by a decrease of total power, attenuation of alpha activity and augmentation of beta activity, as well as by an increase of the centroid and centroid deviation of the total activity. Furthermore, a decrease of the centroid of the combined delta‐theta activity and an increase of the centroid of alpha activity was seen. In contrast, BUS produced an increase of theta activity with an acceleration of the centroid of the combined delta‐theta activity, no modification of alpha activity but a slowing down of its centroid and a tendency to reduce beta activity. The centroid of the total activity was also decreased. Although both compounds have proven their ability to reduce anxiety in patients, their different neurophysiological profiles suggest different neurobiological mechanisms of action after acute administration.

Alterations in Brain Electrical Activity May Indicate the Onset of Malignant Hyperthermia in Swine

The time course of changes in brain electrical activity during halothane anesthesia was examined in 12 malignant hyperthermia-susceptible (MHS) and 14 normal (nMHS) swine. Power densities in selected frequency bands were calculated from the electroen-cephalogram (EEG). EEG and systemic variables were determined over a period of 60 min after starting halothane (1% inspired). Malignant hyperthermia (MH) was triggered in all susceptible pigs. Initial changes in the EEG during development of MH consisted of a decrease in total power and a shift to lower frequencies (delta-theta activity) in all animals. These EEG alterations were noted when there was an increase in heart rate, but other systemic variables were still normal. EEG changes in all MHS animals started at an arterial oxygen tension (PaO2) greater than 90 mmHg and an arterial carbon dioxide tension (PaCO2) less than 50 mmHg. In 5 MHS animals EEG became isoelectric at a PaO2 of 61-82 mmHg and a PaCO2 of 53-68 mmHg. Mean arterial blood pressure at this time was 54-66 mmHg. To determine the effects of hypoxia on the EEG in 7 nMHS animals, oxygen was decreased over a period of 45-60 min to 7% inspired. In 7 other nMHS animals, hypercarbia was produced by admixture of carbon dioxide to the fresh gas supply to achieve incremental increases of PaCO2 to 110-120 mmHg. Significant EEG changes during hypoxia comparable to those seen at the onset of MH were noted at a PaO2 below 40 mmHg and during hypercarbia at a PaCO2 greater than 68 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocorticogram in Rats Loaded with SART Stress (Repeated Cold Stress)

The electrocorticogram (ECoG) in a SART (specific alternation of rhythm in temperature)-stressed (repeatedly cold-stressed) rat, which is regarded as an experimental model for clinical vagotonic-type dysautonomia, was investigated in the present study by the power spectral technique. 1) Analysis of ECoG in SART-stressed rats during the resting-arousal state indicated a decrease in total power and a decrease in relative power in the δ band, and also an increase in relative power in the θ, α and β bands. 2) In the slow-wave sleeping state, the ECoG of SART-stressed rats indicated a marked increase in total power, an increase in the δ band and decreases in θ, α and β bands. 3) Electric stimulation of the posterior-hypothalamic area evoked alterations of ECoG similar to those caused by SART stress. ECoG response to electric stimulation in SART-stressed rats was less than that in unstressed rats. 4) Lesioning of the posterior-hypothalamic areas prevented SART stress-induced ECoG alterations. SART-stressed rats thus appear to be at a higher consciousness level on awakening but to sleep more soundly. They seem to exhibit greater fluctuation in brain activity than normal rats. There is also the possibility that the posterior-hypothalamic area is responsible to some degree for ECoG alterations in SART-stressed rats.

Electrocorticogram in rats loaded with SART stress (repeated cold stress).

The electrocorticogram (ECoG) in a SART (specific alternation of rhythm in temperature)-stressed (repeatedly cold-stressed) rat, which is regarded as an experimental model for clinical vagotonic-type dysautonomia, was investigated in the present study by the power spectral technique. 1) Analysis of ECoG in SART-stressed rats during the resting-arousal state indicated a decrease in total power and a decrease in relative power in the delta band, and also an increase in relative power in the theta, alpha and beta bands. 2) In the slow-wave sleeping state, the ECoG of SART-stressed rats indicated a marked increase in total power, an increase in the delta band and decreases in theta, alpha and beta bands. 3) Electric stimulation of the posterior-hypothalamic area evoked alterations of ECoG similar to those caused by SART stress. ECoG response to electric stimulation in SART-stressed rats was less than that in unstressed rats. 4) Lesioning of the posterior-hypothalamic areas prevented SART stress-induced ECoG alterations. SART-stressed rats thus appear to be at a higher consciousness level on awakening but to sleep more soundly. They seem to exhibit greater fluctuation in brain activity than normal rats. There is also the possibility that the posterior-hypothalamic area is responsible to some degree for ECoG alterations in SART-stressed rats.

Psychophysiological and psychometric studies after manipulating the GABA system by vigabatrin, a GABA-transaminase inhibitor

This study is concerned with the alterations in central and peripheral psychophysiological measures and psychometric variables after experimental manipulation of the most important inhibitory transmitter system of the CNS, the γ-aminobutyric acid (GABA) system. Vigabatrin (GVG), a new enzyme-activated, irreversible inhibitor of GABA transaminase, which increases cerebrospinal fluid concentrations of GABA and other substrates of GABA transaminase, was given in single oral doses of 1 g, 2 g and 3 g to 10 normal healthy volunteers. In this double-blind, placebo-controlled crossover study, 3 mg lorazepam was given as reference compound. Blood sampling for vigabatrin kinetics, EEG recordings and evaluation of pulse, blood pressure and side effects were carried out at the hours 0, 1, 2, 4, 6, 8 and 24, and psychometric tests at the same times (except the first hour). Pharmacokinetic analyses demonstrated good absorption of GVG with peak plasma concentrations found within the first two hours, dose-dependent areas under the plasma concentration-time curves and about 65% recovery in the 24-h urine. Computer assisted spectral analysis of the EEG suggested that GVG procedures only small changes in the normal CNS, characterized by an augmentation of total power, absolute and relative power of the beta activity and acceleration of the centroid of the total activity. There was also a trend towards an increase of alpha activity and of the absolute and relative power of the dominant frequency, decrease in the alpha centroid and increase of the centroid of the combined delta and theta activity. Lorazepam 3 mg, in contrast, produced highly significant changes characterized by a decrease of total power, alpha activity, absolute and relative power of the dominant frequency and centroid of the combined delta and theta activity, while beta activity as well as the centroid of the alpha, beta and total activity increased. In the resting condition an additional augmentation of slow activity suggested hypnotic properties of 3 mg lorazepam. The latter changes are typical for anxiolytic sedatives and were also reflected at the behavioral level where psychometric data demonstrated a deterioration in the noo- and thymopsychic parameters and sedative effects in psychophysiological variables. GVG, on the other hand, produced only subtle changes characterized by an improvement of noo- and thymopsychic variables and vegetative activation.

EEG-Parameter in der Überwachung beatmeter Intensivpatienten unter verschiedenen Sedierungsstrategien

Visual evaluation of the EEG and spectral analysis of the background activity are useful in monitoring changes of cerebral function caused by sedatives, hypoxia and changes in state of health. Continuous slow changes of the EEG are indicative of critical situations of cerebral blood flow or metabolism. Monitoring cerebral function of 40 sedated and ventilated patients on an intensive care unit, we found typical EEG changes dependent on different regimes of sedation, amount of sedatives and patient condition. In patients sedated with etomidate, there was a good correlation between the relative power of the delta and beta-band and patient condition. Sedation with thiopental caused flattening and slowing of the EEG, as well as a decrease of total power, if the doses were increased. The EEG was an aid to predicting the outcome of intensive care and to demonstrate the degree of cerebral damage. In patients with septicaemia, cerebral function was more depressed than in patients with cardiac failure. Spectral analysis and computed parameters proved to be valuable in monitoring cerebral changes caused by sedation and state of health in ventilated patients.

Effects of suriclone on the central neural mechanisms of the respiratory and cardiovascular control systems

The central respiratory and cardiovascular effects of suriclone having an anxiolytic and a hypnotic action were investigated. Experiments were performed on 33 vagotomized rabbits being immobilized and ventilated artificially under monitoring of end-tidal CO2 and O2 levels. The efferent phrenic and renal sympathetic nerve activities were quantitatively studied by means of power spectrum analyses. Suriclone, diazepam or flurazepam in doses of 0.1 and 1 mg/kg i.v. caused respectively a decrease in mean arterial blood pressure ranging from 7 to 17% of the control level after 5 min. The decrease in total power of the phrenic nerve activity in percent to the control 5 min after administration of 0.1 and 1 mg/kg of the 3 drugs, respectively, was: 34+16% (mean+SD, N=9, p<0.01) and 53 + 15% (N=9, p<0.01) after suriclone, 20+22% (N=5) and 41 + 16% (N=10, p<0.01) after diazepam, 7+29% (N=6) and 33 + 19% (N=6, p<0.01) after flurazepam. The percent decrease in total power of the renal sympathetic nerve activity 5 min after 0.1 mg/kg of the 3 drugs was: 32+11% (N=5, p<0.01) after suriclone, 13+8% (N=5, p<0.05) after diazepam, and 3+16% (N=6) after flurazepam. The boundary frequency, at which the direction of response of the phrenic respiratory period to vagal afferent stimulation (0.5V, 0.1msec. 10 to 160Hz) was reversed, was shifted to the lower frequency after suriclone (0.01-5 mg/kg i.v.) as well as diazepam (0.1-5 mg/kg i.v.). In summary, the magnitude of the relative intensity of the centrally mediated hypotensive and respiratory depressant effects of the 3 drugs by intravenous route was in the order of suriclone, diazepam and flurazepam. Furthermore, these results suggest that suriclone as well as diazepam exert a depressant action or. the central integrative mechanisms for the respiratory reflex in the brain stem.