Search PubMed⌕ Search

Biomedical subjects

L Bernardi

Publications and source records attributed to L Bernardi.

At least 91 records · Page 5Linked to original sources

Autonomic control of the heart and peripheral vessels in human septic shock.

OBJECTIVE: Circulating endotoxin impairs the sympathetic regulation of the cardiovascular system in animals. We studied the changes in the autonomic control of the heart and circulation during septic shock in humans. DESIGN: 12 patients (age 43.0 +/- 6, 17-83 years) were investigated during septic shock (mean duration: 3.5 +/- 0.5 days) and during recovery, fluctuations in R-R interval, invasive arterial pressure (AP) and peripheral arteriolar circulation (PC, photoplethysmography) were evaluated by spectral analysis as a validated noninvasive measure of sympathovagal tone. Apache II score was adopted as the disease severity index. Low frequency components (0.03-0.15 Hz) of the frequency spectra were expressed as relative to the overall variability (LFnu) for each cardiovascular variable. RESULTS: LFnu were low or absent during shock but, in the 10 patients who recovered, increased by the time of discharge (post-shock). R-R LFnu increased from 17 +/- 6 to 47 +/- 9 (p < 0.03), AP LFnu from 6 +/- 3 to 35 +/- 4 (p < 0.02) and PC LFnu from 18 +/- 3 to 66 +/- 4 (p < 0.001). Apache II fell from 23.1 +/- 1, at admission, to 14.8 +/- 1.8 at discharge (p < 0.005). Two patients died showing no LFnu increase. CONCLUSION: Reduced LF components of the variability of cardiovascular signals are characteristic of septic shock, confirming the presence of abnormal autonomic control. Restored sympathetic (LF) modulation seems to be associated with a favourable prognosis.

APACHE↗

Physiology and pathophysiology of heart rate and blood pressure variability in humans: is power spectral analysis largely an index of baroreflex gain?

1. It is often assumed that the power in the low- (around 0.10 Hz) and high-frequency (around 0.25 Hz) bands obtained by power spectral analysis of cardiovascular variables reflects sympathetic and vagal tone [corrected] respectively. An alternative model attributes the low-frequency band to a resonance in the control system that is produced by the inefficiently slow time constant of the reflex response to beat-to-beat changes in blood pressure effected by the sympathetic (with or without the parasympathetic) arm(s) of the baroreflex (De Boer model). 2. We have applied the De Boer model of circulatory variability to patients with varying baroreflex sensitivity to patients with varying baroreflex sensitivity and one normal subject, and have shown that the main differences in spectral power (for both low and high frequency) between and within subjects are caused by changes in the arterial baroreflex gain, particularly for vagal control of heart rate (R-R interval) and left ventricular stroke output. We have computed the power spectrum at rest and during neck suction (to stimulate carotid baroreceptors). We stimulated the baroreceptors at two frequencies (0.1 and 0.2 Hz), which were both distinct from the controlled respiration rate (0.25 Hz), in both normal subjects and heart failure patients with either sensitive or poor baroreflex control. 3. The data broadly confirm the De Boer model. The low-frequency (0.1 Hz) peak in either R-R or blood pressure variability) was spontaneously generated only if the baroreflex control of the autonomic outflow was relatively intact.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Sympathetic stimulations by exercise-stress testing and by dobutamine infusion induce similar changes in heart rate variability in patients with chronic heart failure.

1. Heart rate variability can be used to evaluate autonomic balance, but it is unclear how inotropic therapy may affect the findings. The aim of the study was to assess whether heart rate variability can differentiate between sympathetic stimulation induced by inotrope infusion or by physical exercise. 2. Ten patients with chronic heart failure (64.3 +/- 5.4 years of age) underwent four dobutamine infusions (8-min steps of 5 micrograms min-1 kg-1) and four supine bicycle exercise tests (5-min steps of 25 W). Plasma noradrenaline was evaluated, as well as the SD of R-R intervals, together with low-frequency (0.03-0.14 Hz) and high-frequency (0.15-0.4 Hz) components of heart rate variability using autoregressive spectral analysis. 3. Exercise and inotrope infusion produced similar changes in heart rate variability. An exercise load of 50 W and a dobutamine infusion of 15 micrograms min-1 kg-1 gave the following results respectively: heart rate, 120.3 +/- 3.0 beats/min versus 110.2 +/- 3.0 beats/min; SD, 16.0 +/- 1.1 ms versus 16.3 +/- 2.5 ms; low-frequency component, 4.3 +/- 0.3 ln-ms2 versus 4.4 +/- 0.3 ln-ms2 and high-frequency component, 2.6 +/- 0.3 ln-ms2 versus 2.2 +/- 0.3 ln-ms2. All comparisons were nonsignificant. The variables of heart rate variability showed high reproducibility in the same subject during different conditions. Noradrenaline was elevated by exercise from 326.0 +/- 35.2 pg/ml to 860.1 +/- 180.4 pg/ml (P < 0.05), but was unchanged by dobutamine infusion. 4. Heart rate variability changes cannot differentiate between dobutamine infusions and physical exercise, indicating that we should be cautious in evaluating patients undergoing inotropic therapy. The degree of receptor stimulations, rather than the level of sympathetic drive, would appear to determine the changes in heart rate variability.

Aged↗

Determinants of respiratory sinus arrhythmia in the vagotomized rabbit.

After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, beta-adrenergic blockade, and phasic and steady changes in right atrial pressure (RAP) induced by changes in tidal volume (VT, 20, 40, 60 ml), respiratory frequency (RF, 10, 20, 30 cycles/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of variations of the rate of change due to respiration. RSA was assessed by combined autoregressive power spectral analysis of R-R interval and respiration on sequences of 256 heart-beats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P < 0.025 and P < 0.001, respectively) and correlated with dRAP (P < 0.001) and arterial PO2 (P < 0.001). beta-Adrenergic blockade did not change the amplitude of this residual RSA or its dependence on ventilatory mechanics. Dextran-induced increase in mean RAP from 2.9 to 11.9 mmHg did not modify RSA or dRAP. During 100% O2 inhalation, RSA changes were no longer significantly linked to RF and VT, and also the correlation of RSA with dRAP was reduced (P < 0.05). Changing the arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

Autonomic and ventilatory components of heart rate and blood pressure variability in freely behaving rats.

The relative role of parasympathetic, sympathetic, and ventilatory influences in the genesis of blood pressure and R-R interval variability is controversial. In 13 freely behaving WKY rats instrumented with venous and arterial catheters and chest electrodes, mean arterial pressure (MAP, mmHg), R-R interval (ms), and respiratory fluctuations were monitored for 90 min in the control condition and after intravenous atropine (0.75 mg/kg) and/or propranolol (1 mg/kg). Spectral power (pw) in the 0.25- to 0.75-Hz (midfrequency, MF) and the 0.75- to 3.0-Hz (high-frequency, HF, respiratory-synchronous) bands was computed in sequences of 400 heartbeats by use of a combined autoregressive analysis. Atropine reduced but did not abolish HF R-R interval pw (from 1.73 +/- 0.50 to 0.39 +/- 0.27 ms2, P < 0.01) and halved HF MAP pw (from 0.41 +/- 0.30 to 0.21 +/- 0.12 mmHg2, P < 0.05), whereas propranolol did not affect HF pw of the R-R interval or MAP. Propranolol also failed to significantly modify MF R-R interval pw (from 0.48 +/- 0.44 to 0.40 +/- 0.34 ms2, P = NS) or MF MAP pw (from 0.54 +/- 0.39 to 0.42 +/- 0.20 mmHg2, P = NS), whereas atropine virtually abolished MF R-R interval pw (from 0.48 +/- 0.44 to 0.01 +/- 0.01 ms2, P < 0.01) and also significantly reduced MF MAP pw (from 0.54 +/- 0.39 to 0.33 +/- 0.24 mmHg2, P < 0.01). The effects of combined blockade were similar to those of atropine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Flow-diameter phase shift. A potential indicator of conduit artery function.

This study assesses (1) the relation of the very-low-frequency vasomotion (< 0.02 Hz) of the radial artery of young healthy volunteers to regional blood flow and (2) its distribution in the upper extremities. Radial artery diameters from comparable sites were measured on contralateral extremities in 18 young healthy volunteers by an echo tracking system simultaneously with blood flow velocity determined by continuous wave Doppler and blood pressure acquired by photoplethysmography in the middle finger. A synchronous global pattern of vasomotion was detected on contralateral radial arteries, suggesting the presence of either a centrally located pacemaker or a humoral system. Modulation of sympathovagal balance in 8 subjects did not significantly alter either the frequency or amplitude of the very-low-frequency vasomotor waves. Matching patterns of diameter and flow oscillations of the very-low-frequency type recorded at the same site were obtained in 10 strictly nonsmoking volunteers for given periods of time. A consistent phase lag was observed between flow and diameter signals. Flow always preceded the diameter fluctuations by a mean (+/- SEM) course of 20.8 +/- 1.56 seconds. Although the physiological basis for oscillatory behavior remains for the moment highly speculative, these results suggest that the very-low-frequency vasomotion pattern in this conduit vessel might be a flow- or shear stress-dependent phenomenon. Shear stress changes at the endothelium modulate vascular tone through the release of vasodilators. The noninvasive assessment of the diameter-flow relation may thus offer a new way of addressing vascular wall function in medium-sized and large arteries in subjects with cardiovascular risk factors.

Adult↗

[Percutaneous vertebral biopsy. Assessment of results].

The results were reviewed of 81 percutaneous trephine biopsies performed under fluoroscopic or CT guidance from January, 1989, to August, 1994, in 78 patients with thoracic or lumbar vertebral lesions. All the patients presented abnormal findings at conventional radiography and questionable CT or MR findings. A fine-needle sample was obtained as a complementary tool in 9 patients and material for microbiologic culture in 5 patients. Clinical and pathologic findings were correlated for each patient. Biopsy always permitted to obtain sufficient material for the histologic examination; its overall accuracy was 91%. The technique exhibited the highest diagnostic sensitivity in vertebral tumors (100%) and the lowest sensitivity in vertebral infections (69%). Complementary fine-needle sampling was useful especially in small osteolytic lesions, while the microbiologic examination was often negative. There was only one pneumothorax due to the maneuver. To conclude, percutaneous trephine biopsy of thoracic and lumbar spine lesions is a valuable tool for tumor diagnosis which usually spares the patients open surgery.

Adolescent↗

Na+,K+,Cl- cotransport is a marker of distal tubular function in essential hypertension.

OBJECTIVE: To analyze the natriuretic and diuretic response to frusemide in 33 male essential hypertensive patients as a function of basal renal sodium handling and erythrocyte transport system. METHODS: The natriuretic and diuretic response to an oral dose of frusemide (25 mg) was assessed with a simplified method. Urinary sodium and water excretion were measured in the basal state and every 30 min after the frusemide dose for 240 min. Basal 24h urinary sodium and water excretion, Na+,K+,Cl- cotransport and Li+-Na+ countertransport were measured 24 h before the test. RESULTS: There was a highly significant correlation between the natriuretic and diuretic response to frusemide and Na+,K+,Cl- cotransport and Li+-Na+ countertransport. After a multiple regression analysis the natriuretic and diuretic response to frusemide was not correlated with indices of proximal tubular function (Li+-Na+ countertransport, fractional uric acid excretion and the ratio of fractional sodium excretion to fractional uric acid excretion). CONCLUSION: These results support the hypothesis that erythrocyte Na+,K+,Cl- cotransport is a marker of distal tubular function.

Adult↗

Non-respiratory components of heart rate variability in heart transplant recipients: evidence of autonomic reinnervation?

1. Although the high-frequency fluctuations in R-R interval (respiratory sinus arrhythmia) observed in heart transplant recipients are not a reliable marker of reinnervation because of a previously shown direct mechanical effect of breathing, the presence of a non-respiration-related low-frequency oscillation reflects rhythms generated outside the heart, and thus could be neurally mediated. 2. To evaluate the presence of reinnervation, the spontaneous variability in R-R interval was investigated, supine and after passive tilting, in 23 heart transplant recipients (age 43 years, range 23-64 years) and in 25 normotensive control subjects by autoregressive spectral analysis of low- and high-frequency spontaneous fluctuations in R-R interval and respiration. The response of R-R interval to amyl nitrite inhalation was also evaluated in five heart transplant recipients and eight control subjects. 3. Detectable low-frequency oscillations, unrelated to respiration, were present in 13/23 heart transplant recipients, particularly in those who were transplanted at least 20 months earlier (11/14). The natural logarithm of the power of low-frequency fluctuations was markedly lower than in control subjects (0.75 +/- 0.21 versus 5.62 +/- 0.20 ms2, P < 0.001). The low-frequency but not the high-frequency fluctuations correlated with time since transplantation (r = 0.44, P < 0.05). The subjects with low-frequency fluctuations showed a sudden decrease in R-R interval with amyl nitrite linearly related to the decrease in mean blood pressure (r > or = 0.94). The slopes obtained in these heart transplant recipients were comparable (although of lower values) with those obtained in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Low-frequency spontaneous fluctuations of R-R interval and blood pressure in conscious humans: a baroreceptor or central phenomenon?

1. We have tested the hypothesis that the non-respiratory, low-frequency (around 0.1 Hz) fluctuations of heart rate variability are generated by the baroreflexes, but with a delay caused by the slower response of the efferent sympathetic arm, (compared with the vagus), in 11 healthy subjects (mean age +/- SD 27 +/- 5 years). 2. In random order, at the onset of 20 s of apnoea starting at end expiration, we applied either 600 ms neck suction (-40 mmHg) to the carotid sinus region, or no stimulus (anticipation control), or a loud whistle (alerting control), every 60 s, for 30 min. (i.e. 10 of each 'stimulus'). We recorded neck pressure, blood pressure (Finapres), R-R interval (ECG), infra-red plethysmographic skin blood flow and respiration (impedance). By subtracting the alerting response from the neck suction response we obtained the responses caused purely by baroreceptor stimulation. 3. The initial reflex bradycardia and hypotension was followed by arteriolar vasoconstriction, presumably due to recompensation by the baroreflex, and then by a further reflex bradycardia-producing a decaying oscillation of the R-R interval about the control R-R. The period of this damped oscillation was 0.103 +/- 0.024 Hz, similar to the frequency of the low-frequency peak obtained by power spectral analysis of heart rate variability (0.093 +/- 0.016 Hz, not significant) at rest. These two values were significantly correlated in individual subjects (r = 0.715, P < 0.025). 4. These findings support the hypothesis that the low-frequency waves of heart rate variability can be generated from baroreceptor sensed blood pressure fluctuations.

Adult↗

Cardiovascular autonomic modulation in essential hypertension. Effect of tilting.

To better understand the role played by the autonomic nervous system in essential hypertension, we used autoregressive power spectrum analysis to study the noncasual oscillations in RR interval, blood pressure, and skin blood flow in 40 subjects with mild to moderate hypertension and in 25 age-matched control subjects at low frequency (index of sympathetic activity to the heart and the peripheral circulation) and high frequency, respiratory related (index of vagal tone to the heart). RR interval, respiration, noninvasive systolic blood pressure, and skin arteriolar blood flow were simultaneously and continuously recorded with subjects in the supine position and immediately after tilting. The low-frequency component was not significantly different in the two groups either at the cardiac level (control versus hypertensive subjects: 39.1 +/- 4.3 versus 39.9 +/- 3.7 normalized units [NU]) or at the vascular level (1.52 +/- 0.17 versus 1.69 +/- 0.13 ln mm Hg2). After head-up tilting, the RR interval fluctuations were less in hypertensive subjects (low-frequency components from 39.9 +/- 3.7 to 48.4 +/- 4.1 NU, P < .05; high-frequency components from 53.9 +/- 3.7 to 44 +/- 4 NU, P < .05) than in control subjects (low-frequency components from 39.1 +/- 4.3 to 64.4 +/- 4.9 NU, P < .001; high-frequency components from 56.0 +/- 4.5 to 31.2 +/- 4.6 NU, P < .001); the low-frequency components in systolic blood pressure increased similarly in hypertensive subjects (to 2.43 +/- 0.17 ln mm Hg2, P < .0001) and in control subjects (to 2.44 +/- 0.21 ln mm Hg2, P < .01), but the low-frequency components in skin blood flow increased only in control subjects (from 5.34 +/- 0.45 to 6.55 +/- 0.53 mm Hg2, P < .01), not in hypertensive subjects (from 5.55 +/- 0.34 to 5.60 +/- 0.35 ln mm Hg2). In hypertensive subjects with left ventricular hypertrophy, the low-frequency components in systolic blood pressure did not increase after tilting (from 1.75 +/- 0.33 to 2.05 +/- 0.41 ln mm Hg2). Baroreflex sensitivity, as assessed by spectrum analysis, was significantly lower in hypertensive than in control subjects (5.17 +/- 0.49 versus 13.18 +/- 2.44 ms/mm Hg, P < .001. Power spectrum analysis did not reveal an increased sympathetic activity or reactivity either at the cardiac or at the vascular level. The decreased baroreceptor sensitivity in hypertensive subjects could explain the reduced change in sympathovagal balance in the tilt position at the cardiac level. In hypertensive subjects without left ventricular hypertrophy, cardiopulmonary reflex deactivation induced by tilting and/or amplification of sympathetic nervous tone by arteriolar structural change could have preserved the sympathetic activation at the vascular level.

Adolescent↗

Phasic changes in human nasal and skin blood flow: relationship with autonomic tone.

To assess the autonomic control of the microcirculation in human skin and nasal mucosa, the spontaneous fluctuations of a laser Doppler signal recorded on forearm skin and nasal mucosa were compared with heart rate fluctuations and the respiratory signal in 11 healthy subjects by means of spectral analysis. Possible direct mechanical-thermal effects of airflow on the nasal mucosa were evaluated by comparing recordings obtained when the subjects were breathing through either the nose or the mouth. Comparison of the spectral analysis of the signal obtained for skin and nasal mucosa blood flow allowed us to define the characteristics of the autonomic tone of the microcirculation in these two areas. The skin is mainly influenced by sympathetic activity, and the nasal blood flow is regulated by both sympathetic and parasympathetic activity.

Adult↗

[During experimental coronary occlusion dobutamine further slows down the time constant of isovolumetric relaxation].

It has been shown that the time constant (tau) of isovolumic left ventricular (LV) pressure fall is shortened by beta-adrenergic stimulation, possibly reflecting enhanced myocardial relaxation and improved uniformity within the LV wall. Conversely, acute regional ischaemia , slows tau due to mechanical nonuniformity between the nonischaemic and the ischaemic regions. In order to assess the effect of inotropic stimulation on LV pressure fall during acute regional ischaemia, 7 anaesthetized dogs (16 +/- 2 kg) were instrumented with LV and aortic micromanometers. Sonomicrometers were implanted in the areas supplied by the left circumflex and anterior descending arteries to monitor subendocardial segment length (L). After baseline recordings, acute regional ischaemia was induced by 60 s occlusion of the proximal circumflex artery. After a 30 min recovery, the same was repeated during dobutamine infusion (5 micrograms/kg/min). In order to derive tau from heart beats with comparable end-systolic pressures, a caval occlusion run was performed at each stage. The % systolic bulging of the ischaemic zone was defined as: (maximal L--end-diastolic L)/end-diastolic L x 100. The fitting of the exponential model used to derive tau was always good (r > or = 0.99). At comparable end-systolic pressures, tau was increased by acute regional ischaemia (36 +/- 2 versus 32 +/- 2 ms, p < 0.01) and reduced by dobutamine infusion (27 +/- 2 versus 32 +/- 2 ms, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Assessment of regional myocardial performance with end-systolic pressure length and thickness relationships.

Although end-systolic pressure length and thickness relationships (ESPLR, ESPTR) are now widely used as substitutes for the end-systolic pressure volume relationships, there are some reservations about their use as an index of left ventricular (LV) performance. This study addressed three issues, namely: (1) which loading technique (decreasing preload by inferior vena cava (IVC) balloon occlusion or increasing systolic pressure by aortic constriction) is the most likely to yield usable data; (2) reproducibility of these relationships over a 30 min period; and (3) whether by using end-ejection (zero aortic flow) as a definition of end-systole, ESPLR and ESPTR can be used to characterize myocardial performance independent of load. Thirteen anesthetized beagles, weighing 16-25 kg, were used for this study, and were instrumented with sonomicrometers. We found that when ESPLR and ESPTR were constructed from data derived during aortic constriction, the slopes of these relationships were steeper and more curvilinear than when they were constructed from data recorded during IVC occlusion. In addition, the mean between ESPLR, ESPTR obtained 30 min apart was small, although there was a fair degree of variability between the first and second measurements. Using end-ejection to define end-systole, both ESPLR and ESPTR were relatively insensitive to loading conditions (LV end-diastolic pressure of 8-12 mmHg and 14-18 mmHg, aortic systolic pressure of 7-10 mmHg and 20-25 mmHg above baseline (in terms of the slope and shift (leftward or rightward) in these relationships, but were sensitive to inotropic interventions (dobutamine 2.5 micrograms/kg per min and 5 micrograms/kg per min). We conclude that, ESPLR and ESPTR, defined from measurements at end-ejection, can be used as adequate descriptors of regional myocardial performance if they were constructed from data over a similar pressure range during IVC balloon occlusion.

Animals↗

Persistent peripheral vasodilation and sympathetic activity in hypotension after maximal exercise.

Hemodynamics (by aortic Doppler), autonomic factors (power spectrum analysis of heart rate and blood pressure variabilities and baroreceptor sensitivity), and plasma renin activity during the hypotension after maximal exercise were studied in 10 normal subjects on two separate days: a nonexercise (control) day (30 min of upright rest followed by 60 min of supine rest) and an exercise day (maximal upright bicycle exercise followed by 60 min supine) in random order. After exercise, diastolic pressure was reduced for the entire hour, cardiac output increased (+33.8%, P < 0.05), stroke volume was unchanged, and systemic vascular resistance fell (-28.6%, P < 0.01). Indexes of vagal activity were reduced for 60 min, whereas the sympathetic indexes were elevated. Baroreflex sensitivity was also reduced for the first 10 min after exercise. Renin activity increased threefold after exercise. The postexercise hypotension results from a persisting peripheral vasodilation despite an increase in renin activity: the persistent sympathetic activity and reduced vagal tone are probably reflex responses to this vasodilatation.

Adult↗