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Biomedical subjects

G Raimondi

Publications and source records attributed to G Raimondi.

At least 19 recordsLinked to original sources

Positive and negative feedback mechanisms in the neural regulation of cardiovascular function in healthy and spinal cord-injured humans.

BACKGROUND: We tested the hypothesis that in humans, hypertension/tachycardia and hypotension/bradycardia nonbaroreflex sequences that occur within spontaneous arterial pressure (AP) and R-R interval fluctuations are an expression of positive feedback mechanisms neurally regulating the cardiovascular system. METHODS AND RESULTS: We studied 15 spinal cord-injured (SCI) subjects (8 tetraplegics and 7 paraplegics) and 8 healthy subjects. The occurrence of nonbaroreflex (NBseq) and baroreflex (Bseq) sequences, ie, hypertension-bradycardia and hypotension-tachycardia sequences, was assessed during rest and head-up tilt (HUT). The ratio between Bseq and NBseq (B/NB ratio) was also calculated. In resting conditions, the occurrence of NBseq was significantly lower (P:<0.05) in tetraplegics (7.9+/-1.5) than in paraplegics (16.2+/-3.2) and normal subjects (19.0+/-3.5), whereas the occurrence of Bseq was not significantly different between the 3 groups (38.6+/-11.9 versus 45.4+/-6.0 versus 47.0+/-11.9). In tetraplegics, the B/NB ratio showed a marked, significant decrease (from 8.4+/-4.2 to 1.9+/-0.8, P:<0.05) in response to HUT, whereas in normal subjects, it showed a significant increase (from 3.5+/-0.7 to 9.4+/-2.7, P:<0.05). In paraplegics, the B/NB ratio did not change significantly in response to HUT (from 4.5+/-1.6 to 4.8+/-1.1). CONCLUSIONS: Our data suggest that nonbaroreflex sequences occur in humans and might represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation that is able to interact dynamically with feedback mechanisms of baroreflex origin.

Adult↗

Autoreactive isotype-specific T cells determine B cell frequency.

Suppressive activities involving T-B and T-T cell interactions are important to maintain immune system homeostasis. Negative control of IgG2ab+ B cells by anti-IgG2ab T cells derived from Igha mice has been well documented. Nevertheless the real contribution of anti-IgG2ab T cells, endogenously matured in Ighb mice, in controlling IgG2ab+ B cell function has never been investigated. We previously generated anti-IgG2ab TCR-transgenic mice and showed that transgenic T cells were not deleted in the thymus and that they were responsible for a complete and chronic IgG2ab suppression. Here we show that T cells expressing high density of anti-IgG2ab TCR were positively selected in the thymus with a higher efficiency in animals expressing IgG2ab, reached peripheral lymphoid organs and negatively controlled IgG2ab serum levels. Moreover, anti-IgG2ab T cells transgenic for the single TCR chain, thus undergoing normal rearrangements and normal processes of selection, also reached the periphery and suppressed IgG2ab. Interestingly, concentration of IgG2ab in serum inversely correlated with the peripheral frequency of Ig-specific T cells. Finally, T cells able to suppress IgG2ab were obtained from Ighb non-transgenic mice, indicating that anti-2ab T cells are naturally present in the periphery of Ighb animals. We propose that IgG2ab-specific T cells contribute to determine IgG2ab serum levels in Ighb mice.

Animals↗

Average magnitude of heartbeat fluctuations in healthy subjects after exposure to 4 hours head down bed rest.

Orthostatic intolerance, induced by microgravity exposure, has been hypothesized to be related to a disorder of the autonomic control of the cardiovascular system. Non-invasive measurement of Heart Rate Variability (HRV) have been used as a valuable tool to characterize the ability of the autonomic system to modulate the cardiovascular function by analyzing the spontaneous fluctuations of arterial pressure and heart period on a beat-to-beat basis. Concerning this, conflicting results have been reported on the heart rate and blood pressure variability responses during exposure to microG. These differences seem to be due to different experimental designes used. Moreover, the different behavior of normal subjects in response to orthostatic stress after HD, i.e. Symptomatic (S) or Non Symptomatic (NS), could play some role in producing these discrepancies [correction of dicrepancies]. In this study we suggest the analysis of "magnitude" or "volatility" as a new method to study HRV variability. The volatility is a measure of the beat-to-beat excursion capability of the heart, regardless to its direction (positive or negative): the higher the volatility, the greater the excursion. The aim of the present study was to examine R-R volatility before and after 4 hours of HD -6 degrees in normal subjects.

Adult↗

Effects of a residential exercise training on baroreflex sensitivity and heart rate variability in patients with coronary artery disease: A randomized, controlled study.

BACKGROUND: Myocardial ischemia and infarction impair baroreflex sensitivity (BRS), which when depressed is predictive of future cardiac events after myocardial infarction (MI). The main objective of this study was to determine whether exercise training improves BRS in patients with coronary artery disease. METHODS AND RESULTS: Ninety-seven male patients with and without a previous MI were recruited after myocardial revascularization surgery and randomized into trained (TR) or untrained (UTR) groups. TR patients underwent a residential exercise program at 85% of maximum heart rate (HRmax) consisting of 2 daily sessions 6 times a week for 2 weeks. Eighty-six patients (45 TR and 41 UTR) completed the study. BRS was assessed at baseline and at the end of the protocol by the spontaneous baroreflex method. The standard deviation of mean R-R interval (RRSD) was also assessed as a measure of heart rate variability. At baseline, there were no significant differences between TR and UTR patients in any variable. In TR patients, BRS increased from 3.0+/-0.3 to 5.3+/-0.7 ms/mm Hg (P:<0.001), RRSD from 18.7+/-1.4 to 23.6+/-1.6 ms (P:<0.01), and R-R interval from 792. 0+/-15.5 to 851.3+/-20.5 ms (P:<0.001). No significant changes occurred in UTR patients. Increases in BRS and RRSD were significant in patients either with or without a previous MI. CONCLUSIONS: Exercise training increases BRS and heart rate variability in patients with coronary artery disease. Improved cardiac autonomic function might add to the other benefits of exercise training in secondary prevention of ischemic heart disease.

Baroreflex↗

Group III muscle afferents evoke reflex depressor responses to repetitive muscle contractions in rabbits.

Repetitive-twitch contraction of the hindlimb muscles in anesthetized rabbits consistently evokes a reflex depressor response, whereas this type of contraction in anesthetized cats evokes a reflex pressor response in about one-half of the preparations tested. Rapidly conducting group III fibers appear to comprise the afferent arm of the reflex arc, evoking the depressor response to twitch contraction in rabbits because electrical stimulation of their axons reflexly decreases arterial pressure. In contrast, electrical stimulation of the axons of slowly conducting group III and group IV afferents reflexly increases arterial pressure in rabbits. In the present study, we examined the discharge properties of group III and IV muscle afferents and found that the former (i.e., 13 of 20), but not the latter (i.e., 0 of 10), were stimulated by 5 min of repetitive-twitch contraction (1 Hz) of the rabbit triceps surae muscles. Moreover, most of the group III afferents responding to contraction appeared to be mechanically sensitive, discharging in synchrony with the muscle twitch. On average, rapidly conducting group III afferents responded for the 5-min duration of 1-Hz repetitive-twitch contraction, whereas slowly conducting group III afferents responded only for the first 2 min of contraction. We conclude that rapidly conducting group III afferents, which are mechanically sensitive, are primarily responsible for evoking the reflex depressor response to repetitive-twitch contractions in anesthetized rabbits.

Afferent Pathways↗

How is mechanical ventilation employed in the intensive care unit? An international utilization review.

A 1-d point-prevalence study was performed with the aim of describing the characteristics of conventional mechanical ventilation in intensive care units ICUs from North America, South America, Spain, and Portugal. The study involved 412 medical-surgical ICUs and 1,638 patients receiving mechanical ventilation at the moment of the study. The main outcome measures were characterization of the indications for initiation of mechanical ventilation, the artificial airways used to deliver mechanical ventilation, the ventilator modes and settings, and the methods of weaning. The median age of the study patients was 61 yr, and the median duration of mechanical ventilation at the time of the study was 7 d. Common indications for the initiation of mechanical ventilation included acute respiratory failure (66%), acute exacerbation of chronic obstructive pulmonary disease (13%), coma (10%), and neuromuscular disorders (10%). Mechanical ventilation was delivered via an endotracheal tube in 75% of patients, a tracheostomy in 24%, and a facial mask in 1%. Ventilator modes consisted of assist/control ventilation in 47% of patients and 46% were ventilated with synchronized intermittent mandatory ventilation, pressure support, or the combination of both. The median tidal volume setting was 9 ml/kg in patients receiving assist/control and the median setting of pressure support was 18 cm H(2)O. Positive end-expiratory pressure was not employed in 31% of patients. Method of weaning varied considerably from country to country, and even within a country several methods were in use. We conclude that the primary indications for mechanical ventilation and the ventilator settings were remarkably similar across countries, but the selection of modes of mechanical ventilation and methods of weaning varied considerably from country to country.

Data Collection↗

Heart rate and blood pressure response to short-term head-down bed rest: a nonlinear approach.

Although it is well-known that prolonged exposure to microgravity environment such as in space travel results in derangements of orthostasis, recent evidence suggests that even short-term exposure may have similar effects and parallels such common examples as prolonged bed rest. Whereas spectral analysis of heart rate and systolic blood pressure have been unable to detect changes, we hypothesized that nonlinear indexes may be better able to uncover such perturbations. Eighteen healthy subjects were exposed to 4-hour head-down tilt, and of these, 4 exhibited fainting. Two nonlinear indexes, mutual information and recurrence quantification were used to analyze the data. Only recurrence quantification was able to detect a "decoupling" of heart rate and systolic blood pressure at rest using discriminant analysis (p < 0.05). These results suggest that orthostatic intolerance may be due to a decoupling of heart rate from systolic blood pressure reflexive activity occurring at rest.

Adult↗

Effect of 4 hours HD -6 degrees on heart rate variability in symptomatic and non symptomatic subjects.

Orthostatic intolerance is the most serious symptom of cardiovascular deconditioning induced by microgravity exposure. In fact the neural control mechanisms of the cardiovascular system are significantly affected by this condition. Non-invasive measurement of Heart Rate Variability (HRV) have been used as a valuable tool to characterize the ability of neuroendocrine regulatory systems to modulate the cardiovascular function by analyzing the spontaneous fluctuations of arterial pressure and heart period on a beat-to-beat basis. Concerning this, conflicting results have been reported on the heart rate and blood pressure variability responses during exposure to microgravity. These differences seem to be due to different experimental designs used. Moreover, the different behavior of normal subjects in response to orthostatic stress after HD, i.e. Symptomatic (S) or Non Symptomatic (NS), could play some roles in producing these discrepancies. Therefore the aim of the present study was to examine BP and HR variability before and after 4 hours of HD in two groups of normal subjects with and without symptoms of orthostatic intolerance to orthostatic stress.

Adult↗

Muscle metaboreflex contribution to sinus node regulation during static exercise: insights from spectral analysis of heart rate variability.

BACKGROUND: It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia. METHODS AND RESULTS: Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered. CONCLUSIONS: The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation. The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation.

Adult↗

Investigating feed-forward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations.

BACKGROUND: Analysis of spontaneous fluctuations in systolic arterial pressure (SAP) and pulse interval (PI) reveals the occurrence of sequences of consecutive beats characterized by SAP and PI changing in the same (+PI/+SAP and -PI/-SAP) or opposite (-PI/+SAP and +PI/-SAP) direction. Although the former reflects baroreflex regulatory mechanisms, the physiological meaning of -PI/+SAP and +PI/-SAP is unclear. We tested the hypothesis that -PI/+SAP and +PI/-SAP "nonbaroreflex" sequences represent a phenomenon modulated by the autonomic nervous system reflecting a feed-forward mechanism of cardiovascular regulation. METHODS AND RESULTS: We studied anesthetized rabbits before and after (1) complete autonomic blockade (guanethidine+propranolol+atropine, n=13; CAB), (2) sympathetic blockade (guanethidine+propranolol, n=15; SB), (3) parasympathetic blockade (atropine, n=16), (4) sinoaortic denervation (n=10; SAD), and (5) controlled respiration (n=10; CR). Nonbaroreflex sequences were defined as >/=3 beats in which SAP and PI of the following beat changed in the opposite direction. CAB reduced the number of nonbaroreflex sequences (19. 1+/-12.3 versus 88.7+/-36.6, P<0.05), as did SB (25.3+/-11.7 versus 84.6+/-23.9, P<0.001) and atropine (11.2+/-6.8 versus 94.1+/-32.4, P<0.05). SB concomitantly increased baroreflex sensitivity (1.18+/-0. 11 versus 0.47+/-0.09 ms/mm Hg, P<0.01). SAD and CR did not significantly affect their occurrence. CONCLUSIONS: These results suggest that nonbaroreflex sequences represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation able to interact dynamically with the feedback mechanisms of baroreflex origin in the control of heart period.

Animals↗

Effect of postural changes on cardiovascular responses to static exercise in hypertensive human beings.

OBJECTIVE: In hypertensive patients, exaggerated increases in vascular resistance and arterial blood pressure have been reported on changing posture from supine to upright. In this study we tested the hypothesis that in hypertensive subjects, upright posture induces an increase in the vasoconstrictor and pressor responses to physical exercise. SUBJECTS AND METHODS: We studied 17 males with mild hypertension and 10 sex- and age-matched normotensives. Each performed three bouts of static handgrip at 30% maximum voluntary contraction for 2 min after 10 min of supine rest and, in sequence, after 10 min of sitting and 10 min of standing. Arterial pressure, heart rate and forearm vascular resistance were measured by Finapres and plethysmography, respectively. RESULTS: Exercise posture did not affect the mean arterial pressure and heart rate responses to static handgrip. No significant differences in these responses were observed between the hypertensives and the normotensives in any posture. In the hypertensives (n = 12), forearm vascular resistance did not change significantly from resting values during supine and sitting static handgrip but increased significantly during standing static handgrip. In the normotensives, forearm vascular resistance did not change significantly from resting values during static handgrip in any posture. The forearm vascular resistance response to the standing static handgrip was significantly greater in the hypertensives than the normotensives. The algebraic sum of forearm vascular resistance responses to postural change from sitting to standing plus that induced by sitting static handgrip (i.e. additive reflexes) was significantly less than the forearm vascular resistance response to the standing static handgrip (i.e. combined relexes), indicating a facilitatory interaction between exercise and orthostatic stimuli in hypertensives. In contrast, the algebraic sum of the heart rate responses to postural change from sitting to standing plus that induced by sitting static handgrip was significantly greater than the response to standing static handgrip, indicating an inhibitory interaction. CONCLUSIONS: In hypertensive patients, physiological orthostasis causes an increased vasoconstrictor response to static exercise, but this is opposed by an inhibitory influence on the heart rate response, with the result that the pressor response to static exercise is unaffected by upright posture.

Baroreflex↗

Role of muscular factors in cardiorespiratory responses to static exercise: contribution of reflex mechanisms.

We investigated the effects of muscle mass and contraction intensity on the cardiorespiratory responses to static exercise and on the contribution afforded by muscle metaboreflex and arterial baroreflex mechanisms. Ten subjects performed static handgrip at 30% maximal voluntary contraction (MVC) (SHG-30) and one-leg extension at 15% (SLE-15) and 30% (SLE-30) MVC, followed by postexercise circulatory occlusion (PECO). Mean arterial pressure (MAP) and heart rate (HR) responses were greater during SLE-30 than during SHG-30. The difference in MAP was maintained by PECO, and the part of the pressor response maintained by PECO was greater after SLE-30 than after SHG-30 (88.3 +/- 10.6 and 67.8 +/- 12.7%, respectively, P = 0. 02). There were no differences in MAP and HR responses between SHG-30 and SLE-15 trials. Baroreflex sensitivity was maintained during SHG-30 and SLE-15, whereas it was significantly reduced during SLE-30 and recovered back to the resting level during PECO. Minute ventilation and oxygen uptake increased more during SLE-30 than during both SHG-30 and SLE-15 trials. Minute ventilation remained significantly elevated above rest only during PECO following SLE-30. These data suggest that during static exercise the muscle mass and contraction intensity affect 1) the magnitude of the cardiorespiratory responses, 2) the contribution of muscle metaboreflex to the cardiorespiratory responses, and 3) the arterial baroreflex contribution to HR control.

Adult↗

Effect of aging on responses to autonomic cardiovascular tests.

Cardiovascular deconditioning (CD) and orthostatic intolerance represent some of the major disturbances experienced by astronauts returning on Earth after micro-G exposure. The orthostatic intolerance observed in crew members after space missions has been hypothesized to be related to a disorder of the autonomic control of the cardiovascular system. There is evidence that advanced acing itself may alter the cardiovascular mechanism that underlie the CD. Due to involvement of elderly subjects in space flights it is mandatory to verify how age affects the cardiovascular autonomic neural regulation. In order to assess age-related differences in autonomic cardiovascular regulation our aim is to analyze the cardiovascular responses to 3 different autonomic tests that explore baroreceptor (tilt and deep breathing) and non-baroreceptor (isometric exercise) afferent pathways, in two goups of normal subjects characterized by significant different age.

Adolescent↗

Peripheral vascular changes after short-term simulated microgravity.

Cardiovascular deconditioning and orthostatic intolerance are the main symptoms experienced by astronauts after space flights. Alterations in the cardiovascular neural regulation have been implicated in the genesis of these disorders, but the mechanisms have not been clearly established. Alterations in the reflex control of circulation from the arterial and cardiopulmonary baroreceptive areas have been mainly hypothesized on the basis of long-term simulated microgravity studies. However, symptoms of orthostatic intolerance, and even fainting, are also observed after short-term exposure to simulated micro-G conditions. The possibility does exist that short-term exposure to micro-G conditions could affect the cardiovascular regulation differently from long-term exposure. Previous studies from this laboratory have shown that arterial baroreflex control of heart rate is not altered after 4 hours Head Down (HD) at -6 degrees, whereas it is significantly decreased after 28 days. Again, the role played by possible disturbances of the vasomotor regulation in the genesis of orthostatic intolerance after short term exposure to simulated microgravity has not yet been clarified. The aim of this study was therefore to evaluate peripheral blood flow changes following 2 and 4 h HD -6 degrees in healthy volunteers.

Adult↗

[Spontaneous baroreflex control of heart rate during chronic tandropril therapy].

Differently from other vasodilators, the antihypertensive effect of ACE-inhibitors is not accompanied by an increase in resting heart rate which suggests a modulatory action of these drugs on arterial baroreflex control of heart rate. It is debated whether this modulation involve, an increase in gain (or sensitivity) of baroreflex mechanisms controlling heart rate or is due to a baroreflex control resetting. In this study we investigated the arterial baroreflex control of heart rate both in supine rest and during active standing before and after 7 and 30 days of treatment with a new ACE-inhibitor, trandolapril (2 mg per os oid) in 15 mild hypertensive patients. Baroreflex control of heart rate has been dynamically and non-invasively assessed by analysis of the continuous relationship between beat-to-beat spontaneous fluctuations in systolic blood pressure and pulse interval. By this method, sequences of 3 or more consecutive beats in which systolic blood pressure and pulse interval change in the same direction (either increasing or decreasing) are identified and a linear regression is applied to each individual sequence. The mean individual slope of the systolic blood pressure/pulse interval ratio obtained by averaging all slopes computed within a given period, is calculated and taken as an estimate of the spontaneous baroreflex sensitivity for that period. Trandolapril reduced resting blood pressure significantly (from 147.5 +/- 3.3/95.3 +/- 1.5 to 129.5 +/- 3.7/83.6 +/- 1.6 and 126.6 +/- 3.9/84.5 +/- 1.7 mmHg after 7 e 30 days, respectively) without affecting heart rate. The treatment did not alter baroreflex sensitivity but resulted in an apparent leftward shift of the regression line relating systolic blood pressure to pulse interval along the pressure axis, reflecting the lower prevailing level of arterial pressure. The increases in heart rate and blood pressure induced by standing in control conditions were not significantly modified by trandolapril. Baroreflex sensitivity was significantly reduced by standing both in control conditions and, to the same extent, during treatment. These results suggest that ACE-inhibition does not alter the gain of the integrated baroreflex mechanisms controlling heart rate, but results in a baroreflex resetting that may explain the lack of tachycardia normally observed during antihypertensive therapy with ACE-inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗

Effects of isokinetic, isotonic and isometric submaximal exercise on heart rate and blood pressure.

The purpose of the present study was to compare arterial pressure (AP) and heart rate (HR) responses to submaximal isokinetic, isotonic and isometric exercises currently employed in physical rehabilitation therapy in terms of both magnitude and time-course. To this aim AP and HR were continuously and noninvasively measured in ten healthy subjects performing isokinetic, isotonic and isometric exercises at the same relative intensity. Isokinetic and isotonic exercises consisted of 30 knee extension/flexion repetitions at 40% of maximal effort. Isokinetic speed was set at 180 degrees s(-1). Isometric exercise consisted of a 60-s knee extension at 40% maximal voluntary contraction. The AP showed a rapid and marked increase from the onset of all types of exercise progressing throughout the exercises. Peak systolic (SAP) and diastolic (DAP) arterial pressure were 190.7 (SEM 8.9) and 121.6 (SEM 7.8) mmHg during isokinetic and 197.6 (SEM 11.2) and 128.3 (SEM 7.7) mmHg during isotonic exercise, respectively. During isometric exercise peak SAP and DAP were 168.1 (SEM 6.3) and 102.1 (SEM 3.7) mmHg, respectively [both lower compared to isokinetic and isotonic exercise (P < 0.05)]. The HR rose abruptly and after five isokinetic and isotonic repetitions it had already increased by about 30 beats min(-1), continuing to rise throughout the exercises. The HR response to isometric exercise was significantly less (P < 0.05) at all times. An immediate fall in AP, undershooting resting levels, was observed at the cessation of all types of exercise, being more marked after isokinetic and isotonic exercise. These results indicate that submaximal exercise of a dynamic type induces greater AP responses than intensity-matched isometric exercise and that even submaximal endurance-type rehabilitation exercise yields an elevated functional stress on the cardiovascular system which could precipitate hazardous events particularly in subjects with unrecognized cardiac diseases.

Adult↗

Baroreflex control of sinus node during dynamic exercise in humans: effects of central command and muscle reflexes.

This study evaluated the influence of central command and muscle afferent stimulation (mechanical and chemical) on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Twenty-two healthy men performed voluntary knee extension and electrically induced dynamic knee extension under free-flow and arrested-flow (n = 18) conditions. Systolic arterial pressure (SAP) and pulse interval (PI) were measured continuously and noninvasively. The arterial baroreflex was evaluated by analyzing the slopes of sequences of three or more consecutive beats characterized by the SAP and PI of the following beat; both increased or decreased in a linear fashion. Compared with rest, both voluntary exercise and electrically induced exercise under arrested-flow conditions resulted in a maintained baroreflex sensitivity (BRS; 11.7 +/- 1.2 vs. 9.6 +/- 0.7 and 11.3 +/- 1.4 vs. 9.8 +/- 1.5 ms/mmHg, respectively; not significant), with an apparent rightward shift in the regression line relating SAP to PI. Electrically induced exercise under free-flow conditions resulted in a significant decrease in BRS (12.1 +/- 1.4 vs. 8.8 +/- 0.8 ms/mmHg; P < 0.05). These data suggest that the central command and muscle chemoreflex act to preserve the BRS, possibly "resetting" the baroreceptor-cardiac response relationship, whereas stimulation of mechanosensitive receptors appears capable of modifying the integrated baroreflex control of sinus node function in humans. The first two mechanisms seem, however, to overwhelm the latter to maintain BRS, thus permitting a concomitant increase in arterial pressure and heart rate.

Adult↗

Evaluation of reproducibility of spontaneous baroreflex sensitivity at rest and during laboratory tests.

OBJECTIVE: The aim of the present study was to examine the reproducibility of arterial baroreflex sensitivity (BRS) provided by the spontaneous baroreflex method at rest and during laboratory tests. METHODS: Twenty healthy volunteers were studied 24 h apart, in the same laboratory and under the same environmental conditions, at rest, during active standing, while performing mental arithmetics and during static hand-gripping. Systolic blood pressure, mean arterial pressure and pulse interval were continuously and non-invasively measured by using a Finapres device. BRS was evaluated by analysing the slopes of spontaneously occurring sequences of three or more consecutive beats in which systolic blood pressure and pulse interval of the following beat both increased or decreased, in the same direction, in a linear fashion. Individual BRS were obtained by averaging all slopes computed within a given test. RESULTS: Under each test condition BRS did not differ significantly between the two consecutive days, showing strikingly similar values. The mean group coefficients of variation (CVAR), obtained by averaging individual CVAR, between the two experimental days were 15.0, 13.9 and 19.7% for resting, standing, static hand-gripping and mental arithmetic, respectively. No relationships were found between individual CVAR and individual mean arterial pressure, pulse interval and number of baroreflex sequences under any tested condition, on both experimental days. CONCLUSIONS: These results show that the spontaneous baroreflex method provides good BRS reproducibility under various stimuli that affect the neural control of circulation differently. They also suggest that BRS variability is dependent neither on haemodynamic modifications nor on the degree of baroreflex engagement, but it seems to reflect an inherent feature of the way in which arterial baroreflex modulate the heart period.

Adult↗