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Biomedical subjects

A Malliani

Publications and source records attributed to A Malliani.

At least 19 recordsLinked to original sources
PubMed1995

Adenosine activates cardiac sympathetic afferent fibers and potentiates the excitation induced by coronary occlusion.

Adenosine is a possible mediator of cardiac pain during myocardial ischemia; however, little is known about the influence of adenosine on cardiac sympathetic afferent activity and thereby on its algogenic mechanism. In 20 anaesthetized, decerebrated, curarized and artificially ventilated cats, we studied the impulse activity of 20 single afferent sympathetic fibers with a left ventricular receptive field in relation to epicardial applications of adenosine, coronary artery occlusions and arterial pressure rises. All fibers increased their impulse activity (from 1.2 +/- 0.2 to 2.6 +/- 0.5 imp/s; P < 0.001) during slight (20 +/- 8%) rises in aortic pressure, thus exhibiting low-threshold receptor characteristics. In 10 cats, epicardial applications of three different doses of adenosine (0.1, 1 and 10 mg/ml) caused a brief increase in neural activity with dose-related responses. This response was abolished by aminophylline, a P1 purinergic inhibitor. In the other group of 10 cats, four subsequent 30-s occlusions of the coronary arterial vessel supplying the receptive fields of the fibers were performed, in control conditions and 30 s, 3 and 7 min, respectively, after the end of excitation induced by adenosine (1 mg/ml) application. During the control coronary occlusion the impulse activity increased from 1.1 +/- 0.1 to 5.5 +/- 0.7 imp/s (P < 0.0001). A similar activation was present during the second occlusion initiated 30 s after the end of adenosine-induced activation. In contrast, a significant potentiation of the response was observed (8.8 +/- 1.2 vs. 5.3 +/- 0.9 imp/s; P < 0.001) during the occlusion initiated 3 min after the end of excitation by adenosine. This effect was no longer present during the last occlusion performed after 7 min. When the protocol was repeated substituting adenosine with saline (n = 5) or after i.v. administration of aminophylline (n = 5), no potentiation was observed, even though the excitatory response to coronary occlusion was preserved. These data show that adenosine can activate cardiac sympathetic afferent fibers in a dose-related manner, and potentiate their responses to coronary occlusion, while leaving unaffected the responsiveness to a hemodynamic stimulus. The excitatory effects are likely to involve the P1 purinergic receptors. The potentiation phenomenon might play a role in the genesis of an algogenic code.

Adenosine↗
PubMed1995

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 degrees, 60 degrees, 90 degrees) 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 degrees 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, LFRR) and vagal (high-frequency oscillations, about 0.25 Hz, HFRR) modulations of heart period and of sympathetic vasomotor activity (low-frequency oscillations of SAP variability, LFSAP). Baroreceptor mechanisms were quantified by means of the index alpha (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 LFRR and LFSAP components. Moreover, HFRR, 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.

Atropine↗
PubMed1994

Effects of beta blockers (atenolol or metoprolol) on heart rate variability after acute myocardial infarction.

This study analyzed, with spectral techniques, the effects of atenolol or metoprolol on RR interval variability in 20 patients 4 weeks after the first uncomplicated myocardial infarction. Beta blocker-induced bradycardia was associated with a significant increase in the average 24-hour values of RR variance (from 13,886 +/- 1,479 to 16,728 +/- 1,891 ms2) and of the normalized power of the high-frequency component (from 22 +/- 1 to 28 +/- 2 normalized units), whereas the low-frequency component was greatly reduced (from 60 +/- 3 to 50 +/- 3 normalized units). When considering day and nighttime separately, the effects of both drugs were more pronounced in the daytime. In addition, a marked attenuation was observed in the circadian variation of the low-frequency component after beta blockade. As a result, the early morning increase of the spectral index of sympathetic modulation was no longer detectable. These results indicate that beta-blocker administration has important effects on RR interval variability and on its spectral components. The observed reduction in signs of sympathetic activation and the increase in vagal tone after beta blockade help to explain the beneficial effects of these drugs after myocardial infarction. However, the potential clinical relevance of the increase in RR variance remains to be established.

Atenolol↗
PubMed1994

Model for the assessment of heart period and arterial pressure variability interactions and of respiration influences.

A model which assesses the closed-loop interaction between heart period (HP) and arterial pressure (AP) variabilities and the influence of respiration on both is applied to evaluate the sources of low frequency (LF approximately 0.1 Hz) and high frequency (HF, respiratory rate approximately 0.25 Hz) in conscious dogs (n = 18) and humans (n = 5). A resonance of AP closed-loop regulation is found to amplify LF oscillations. In dogs, the resonance gain increases slightly during baroreceptor unloading (mild hypotension obtained with nitroglycerine (NTG) i.v. infusion, n = 8) and coronary artery occlusion ((CAO), n = 6), and it is abolished by ganglionic transmission blockade ((ARF), Arfonad i.v. infusion, n = 3). In humans, this gain is considerably increased by passive tilt. Different, possibly central, sources of LF oscillations are also evaluated, finding a strong rhythmic modulation of HP during CAO. At HF, a direct respiratory arrhythmia is dominant in dogs at control, while it is considerably reduced during CAO. On the contrary, in humans, a strong influence of respiration on AP is shown which induces a reflex respiratory arrhythmia. An index of the gain of baroreceptive response, alpha cl, was decreased by NTG and CAO, and virtually abolished by chronic arterial baroreceptive denervation (TABD, n = 4) and ARF.

Animals↗
PubMed1994

Sympathetic restraint of baroreflex control of heart period in normotensive and hypertensive subjects.

1. We assessed the effects of changing levels of sympathetic drive on the gain of baroreflex control of the sino-atrial node, in normotensive and hypertensive subjects. 2. Autoregressive spectral and cross-spectral analysis of R-R interval and systolic arterial pressure (non-invasive Finapres method) variabilities providing an estimate of baroreflex gain through the frequency domain index alpha were performed on data from 63 normotensive and 78 mild hypertensive subjects. Subjects were studied at rest and during active orthostatism, which induces sympathetic predominance. Seven control subjects and 14 hypertensive subjects were also studied after chronic atenolol treatment, to attenuate beta-adrenoceptor-mediated responses. 3. In both normotensive and hypertensive subjects, the index alpha was reduced by active standing and increased by chronic beta-adrenoceptor blockade. Furthermore, at rest, the index alpha was correlated with R-R variance and appeared significantly reduced with age. The age-related negative correlation of the index alpha was no longer evident during the standing-induced increase in sympathetic drive, in both normotensive and hypertensive subjects. 4. The index alpha, a non-invasive frequency domain estimate of the overall gain of baroreflex control of the sino-atrial node, which appears to be reduced in essential hypertension, is negatively modulated by physiological increases in sympathetic drive, and augmented by pharmacological blockade of beta-adrenoceptors. 5. In essential hypertension the enhanced sympathetic drive present already at rest, and the simultaneous reduction of the gain of baroreflex mechanisms, are the expression of a complex alteration in neural cardiovascular control.

Adult↗
PubMed1994

Sympathetic overactivity in subjects complaining of unexplained fatigue.

1. Theoretical and practical considerations suggest that in subjects complaining of fatigue, in the absence of evident organ dysfunction, an alteration in the autonomic nervous system might be present as a functional correlate. 2. Autoregressive spectral analysis of R-R interval variability from a surface ECG, was used in healthy control subjects (n = 24, age 45 +/- 4 years) and in subjects complaining of unexplained fatigue (n = 53, age 46 +/- 9 years) to obtain quantitative indices of the state of the sympathovagal balance, both at rest and during a mental stimulus (mental arithmetic), capable of enhancing sympathetic drive. Sympathetic and vagal modulations were inferred from the normalized powers of the low frequency and high frequency spectral components respectively. 3. We observed in patients, at rest, a prevailing low frequency component of R-R variability (patients low frequency = 73 +/- 11, control subjects 51 +/- 10 normalized units, P < 0.05). The responsiveness to mental arithmetic was reduced in patients as compared with controls. Systolic blood pressure variability did not differ. This suggested a selective imbalance in autonomic control of the sinoatrial node, characterized by sympathetic predominance as well as by vagal withdrawal, at rest. 4. The possibility of discriminating patients from control subjects on the basis of simple non-invasive functional markers might provide a better understanding of the mechanisms, clinical evolution and outcome of conditions such as the chronic fatigue syndrome, which lack ordinary evidence of disease, but comprise, as physiopathological correlate, a quantitative alteration of autonomic control.

Autonomic Nervous System↗
PubMed1994

Restraining effects of captopril on sympathetic excitatory responses in dogs: a spectral analysis approach.

This study was planned to clarify the effects of captopril administration on the autonomic control of the circulation in conscious dogs and in dynamic conditions using spectral analysis of R-R interval and systolic arterial pressure (SAP) variabilities. Changes in sympathovagal balance modulating the sinoatrial (SA) node were inferred, respectively, from the low (LFR-R)- and high-frequency (HFR-R) components of R-R variability; LFSAP furnished a marker of sympathetic vasomotor control. Increases in sympathetic activity were induced by three different experimental maneuvers [bilateral carotid occlusion (BCO), coronary artery occlusion (CAO), and dynamic exercise] capable of increasing sympathetic outflow to the SA node and to the vessels. Studies were performed both before and after intravenous captopril administration. During BCO, only LFSAP increased from 4.3 +/- 1.5 to 19.7 +/- 4.1 mmHg2; during CAO, both LFR-R and LFSAP increased, respectively, from 3 +/- 1 to 21 +/- 2 normalized units (nu) and from 4.1 +/- 1.3 to 7.2 +/- 1.5 mmHg2. Dynamic exercise at 2 and 4 km/h progressively raised LFR-R from 8 +/- 2 to 58 +/- 7 and 75 +/- 5 nu, respectively; LFSAP showed a parallel trend increasing from 2.5 +/- 0.7 to 8.04 +/- 1.9 and 12.7 +/- 2.2 mmHg2. In all experimental conditions, captopril significantly (P < 0.05) blunted the increase of LFSAP. A restraining effect on LFR-R was apparent only with CAO. Spectral analysis of cardiovascular variabilities indicates that, in the conscious dog, acute captopril administration has an important inhibitory effect on cardiac sympathetic excitatory mechanisms as well as on sympathetic vasomotor control.

Animals↗
PubMed1994

Power spectrum analysis of heart rate variability to assess the changes in sympathovagal balance during graded orthostatic tilt.

BACKGROUND: The powers of the low-frequency (LF) and high-frequency (HF) oscillations characterizing heart rate variability (HRV) appear to reflect, in their reciprocal relationship, changes in the state of the sympathovagal balance occurring during numerous physiological and pathophysiological conditions. However, no adequate information is available on the quantitative resolution of this methodology. METHODS AND RESULTS: We studied 22 healthy volunteers (median age, 46.5 years) who were subjected after a rest period to a series of passive head-up tilt steps randomly chosen from the following angles: 15 degrees, 30 degrees, 45 degrees, 60 degrees, and 90 degrees. From the continuous ECG, after appropriate analog-to-digital conversion, a personal computer was used to compute, with an autoregressive methodology, time and frequency domain indexes of RR interval variability. Spectral and cross-spectral analysis with the simultaneously recorded respiratory signal excluded its contribution to LF. Age was significantly correlated to variance and to the absolute values in milliseconds squared of very-low-frequency (VLF), LF, and HF components. The tilt angle was correlated to both LF and HF (expressed in normalized units [nu]) and to the LF-to-HF ratio (r = .78, -.72, and .68; respectively). Lower levels of correlation were found with HF (in ms2) and RR interval. No correlation was present between tilt angle and variance, VLF, or LF (in ms2). Individual analysis confirmed that the use of nu provided the greatest consistency of results. CONCLUSIONS: Spectral analysis of HRV, using nu or LF-to-HF ratio, appears to be capable of providing a noninvasive quantitative evaluation of graded changes in the state of the sympathovagal balance.

Adult↗
PubMed1994

[Methods for assessing the autonomic nervous system in man].

Assessment of baroreflex sensitivity and spectral analysis of heart rate variability are two methods capable of providing relevant information on neural mechanisms controlling heart period and on their alterations during several pathophysiological conditions such as coronary artery disease and cardiac insufficiency. These techniques provide complementary information: the former is based on a stimulus-response model which has in the activation of vagal fibers directed to the heart its main efferent component; the latter, by quantifying the spontaneous harmonic oscillations of heart period, furnishes indices of sympathetic and vagal modulation of sinus node.

Autonomic Nervous System↗
PubMed1993

[Behavior, sympathetic nervous system, and arterial hypertension].

The discharge of sympathetic and vagal outflows appears regulated, in general, by a reciprocal interaction, that is to say that the increased activity of one component is accompanied by the decreased activity of the other. A sympathetic excitation can depend on central neural mechanisms, on peripheral excitatory reflexes and on a reduced inhibition exerted by inhibitory reflex mechanisms. Behavioral studies can reveal conditions associated with an increased sympathetic activity and with an augmented arterial pressure. The use of a spectral methodology applied to the study of cardiovascular variability allows the quantification, on the whole, of the state of sympatho-vagal balance: in the course of essential arterial hypertension this equilibrium appears shifted towards a sympathetic predominance.

Behavior↗
PubMed1992

Circadian variation of spectral indices of heart rate variability after myocardial infarction.

The circadian variations of spectral indices of heart rate variability were analyzed in 20 patients 4 weeks after a first and uncomplicated myocardial infarction (MI) and in 20 control subjects. R-R interval and variance showed a characteristic day-night pattern with a significant reduction of the latter parameter in patients after MI (10,967 +/- 1109 msec2 vs 16,860 +/- 2132 msec2). Control subjects were characterized by a predominance of low-frequency (approximately 0.1 Hz) component during the day and of high-frequency (approximately 0.25 Hz) component during the night, which reflected the expected 24-hour pattern of variation of sympatho-vagal balance. A 24-hour elevation (64 +/- 3 normalized units [nu] vs 56 +/- 2 nu; p less than 0.05) of the low-frequency component and a smaller (23 +/- 2 nu vs 32 +/- 2 nu; p less than 0.05) high-frequency component during the night differentiated patients after MI from subjects. The difference between the two groups was even more evident when the 24-hour sympatho-vagal balance was assessed with the low frequency/high frequency ratio. Thus spectral analysis of heart rate variability indicates that in patients after MI there is an alteration of neural control mechanisms as indicated by the presence of signs of sympathetic activation and by the attenuation of the nocturnal increase in vagal tone.

Aged↗
PubMed1992

Spectral analysis of sympathetic discharge, R-R interval and systolic arterial pressure in decerebrate cats.

In 19 decerebrate and artificially ventilated cats, we analyzed, with a power spectral methodology, the variability simultaneously present in R-R interval and in thoracic preganglionic sympathetic outflow. R-R interval was characterized, as already described in humans and other experimental preparations, by two rhythmic components occurring at a frequency of about 0.1 Hz (low-frequency, LF) and at one corresponding to respiratory rate (high-frequency, HF) which, in these experiments, was set at 0.32 Hz. Two similar rhythmic components were also present in the sympathetic discharge. Arterial pressure changes were produced by aorta or vena cava flow obstruction in order to produce reflex responses in sympathetic activity. Reflex sympathetic excitations induced an increase in the LF component of both R-R interval and sympathetic discharge variabilities, while the HF components were simultaneously reduced. In contrast, reflex sympathetic inhibitions were accompanied by a decrease in LF components of both variability signals, while the HF components were simultaneously increased. A significant and positive correlation was found between changes in impulse activity and the amplitude of LF component of either R-R interval or sympathetic discharge variabilities. These data support the hypothesis that the low-frequency component of R-R variability can be used as a marker of sympathetic modulation.

Animals↗
PubMed1992

Effects of chronic cilazapril treatment on cardiovascular control: a spectral analytical approach.

In 11 subjects with mild hypertension (sitting arterial pressure of 146 +/- 5/97 +/- 2 mm Hg), the effects of chronic angiotensin-converting enzyme (ACE) inhibition (cilazapril, 5 mg p.o. once daily for 4 weeks) were studied at rest and during active standing by means of spectral analysis. Sympathetic vascular control was inferred from the power of the low-frequency (LF) component of the systolic arterial pressure (SAP) variability, assessed noninvasively with a plethysmographic technique. Simultaneously, quantitative indices of neural control of the sinoatrial (SA) node were obtained with the power of the LF and of the high-frequency (respiration linked) component of R-R variability. Before treatment, active standing produced a clear increase in the LF components of R-R and SAP variabilities. At the end of the 4 weeks of cilazapril treatment, the LF component of SAP variability during standing was significantly lower than prior to treatment, while the increase in the LF component of R-R variability was left unchanged. These findings suggest an inhibitory effect of chronic ACE inhibition upon vasomotor sympathetic control, as assessed non-invasively by this technique.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Analysis of neural mechanisms accompanying different intensities of dynamic exercise.

The neural mechanisms accompanying dynamic exercise of different intensities were analyzed in dogs and human subjects by means of autoregressive spectral analysis of heart period and arterial pressure variabilities. In the animal experiments, 8 conscious dogs were examined after implanting a solid state pressure gauge in the left ventricle. Animals were examined at rest and during a treadmill run, at 4 km/h, and 0 degrees incline. The experiments were repeated after chronic alpha 1-adrenoreceptor blockade. During the treadmill run, heart rate and systolic left ventricular pressure increased significantly. Simultaneously, the low frequency (LF, 0.1 Hz) component of pulse interval and of systolic pressure variabilities, ie, markers, respectively, of sympathetic modulation of the SA node and of vasomotor activity, increased significantly (evaluated respectively, in normalized and absolute units). After chronic alpha 1-adrenoreceptor blockade, the increase in LF component of systolic pressure variability was prevented, while that observed in R-R interval variability was maintained. Human studies were carried out with either invasive or noninvasive techniques. In the former approach already described, performed in young hypertensive subjects, arterial pressure was recorded with a high fidelity technique. In the second approach applied to young champion swimmers, only the variability of the R-R interval was examined. In both studies, moderate levels of exercise were accompanied by an increase in the LF component of the spectrum: in the case of arterial pressure variability, this increase was detectable both in absolute and normalized units; vice versa, in the case of R-R variability, since physical exercise is accompanied by a marked abatement of the variance, normalized units had to be used in order to evaluate the shift of the sympathovagal balance in favor of sympathetic overactivity.

Adolescent↗