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Biomedical subjects

Luciano Bernardi

Publications and source records attributed to Luciano Bernardi.

16 recordsLinked to original sources
PubMed2007

Reduced hypoxic ventilatory response with preserved blood oxygenation in yoga trainees and Himalayan Buddhist monks at altitude: evidence of a different adaptive strategy?

Yoga induces long-term changes in respiratory function and control. We tested whether it represents a successful strategy for high-altitude adaptation. We compared ventilatory, cardiovascular and hematological parameters in: 12 Caucasian yoga trainees and 12 control sea-level residents, at baseline and after 2-week exposure to high altitude (Pyramid Laboratory, Nepal, 5,050 m), 38 active lifestyle high-altitude natives (Sherpas) and 13 contemplative lifestyle high-altitude natives with practice of yoga-like respiratory exercises (Buddhist monks) studied at 5,050 m. At baseline, hypoxic ventilatory response (HVR), red blood cell count and hematocrit were lower in Caucasian yoga trainees than in controls. After 14 days at altitude, yoga trainees showed similar oxygen saturation, blood pressure, RR interval compared to controls, but lower HVR (-0.44 +/- 0.08 vs. -0.98 +/- 0.21 l/min/m/%SaO(2), P < 0.05), minute ventilation (8.3 +/- 0.9 vs. 10.8 +/- 1.6 l/min, P < 0.05), breathing rate (indicating higher ventilatory efficiency), and lower red blood cell count, hemoglobin, hematocrit, albumin, erythropoietin and soluble transferrin receptors. Hypoxic ventilatory response in monks was lower than in Sherpas (-0.23 +/- 0.05 vs. -0.63 +/- 0.09 l/min/m/%SaO(2), P < 0.05); values were similar to baseline data of yoga trainees and Caucasian controls, respectively. Red blood cell count and hematocrit were lower in monks as compared to Sherpas. In conclusion, Caucasian subjects practicing yoga maintain a satisfactory oxygen transport at high altitude, with minimal increase in ventilation and with reduced hematological changes, resembling Himalayan natives. Respiratory adaptations induced by the practice of yoga may represent an efficient strategy to cope with altitude-induced hypoxia.

Acclimatization↗
PubMed2006

Effects of physical training on cardiovascular control after heart transplantation.

BACKGROUND: Exercise performance in heart-transplanted patients increases with respect to pre-transplantation but remains subnormal, and it does not improve with time after surgery. Possible causes include persisting denervation, and sympathetic vasoconstriction inducing functional vascular abnormalities that prevent adequate increase in blood flow to the exercising limbs. We tested the effects of physical training on baroreceptors-mediated control of heart rate and blood pressure in recently heart-transplanted subjects. METHODS: Patients were randomly allocated to physical training (n=13, 30 min cycling at 60-70% of peak oxygen consumption for 5 days/week for 6 months) or to control (n=11). Upright exercise test to exhaustion was performed at the beginning of the study after 3 and 6 months. Reflex changes in RR interval and blood pressure in response to sinusoidal neck suction (6 and 12 cycles/min 0 to -30 mm Hg swing) were considered as evidence of reinnervation and baroreflex control of blood pressure, respectively. RESULTS: After 6 months peak oxygen consumption (p<0.001), exercise time (p<0.01) and workload (p<0.01) increased in trained patients. Before training RR interval and blood pressure were not modified by neck suction. After physical training systolic (p<0.01) and diastolic blood pressure decreased, RR interval and blood pressure could be modulated (p<0.05) by slow (6 cycles/min) neck suction, indicating initial cardiac sympathetic reinnervation and restored sensitivity to autonomic modulation on the arteries. No changes were observed in controls. CONCLUSIONS: Physical training improved exercise performance and the control exerted by the autonomic nervous system through the sympathetic nerves at both cardiac and vascular level.

Adult↗
PubMed2006

Effect of treatment with nasal continuous positive airway pressure on ventilatory response to hypoxia and hypercapnia in patients with sleep apnea syndrome.

BACKGROUND: The increase in peripheral chemoreflex sensitivity in patients with obstructive sleep apnea (OSA) is associated with activation of autonomic nervous system and hemodynamic responses. Nasal CPAP (nCPAP) is an effective treatment for OSA, but little is known on its effect on chemoreflex sensitivity. OBJECTIVES: To assess the effect of nCPAP treatment or placebo (sham nCPAP) on ventilatory control in patients with OSA. SETTING: Sleep laboratory of Azienda Ospedaliera Garibaldi. PATIENTS: Twenty-five patients with moderate-to-severe OSA. DESIGN AND MEASUREMENTS: Patients were randomly assigned to either therapeutic nCPAP (use of optimal pressure, n = 15) or sham nCPAP (suboptimal pressure of 1 to 2 cm H2O, n = 10) in a double-blind fashion and treated for 1 month. A rebreathing test to assess ventilatory response to normocapnic hypoxia and normoxic hypercapnia was performed at basal condition and after 1 month of treatment. RESULTS: The use of therapeutic nCPAP or sham nCPAP did not affect daytime percentage of arterial oxygen saturation (SaO2%) or end-tidal P(CO2). The normocapnic hypoxic ventilatory response was reduced after 1 month of treatment with nCPAP (the slope was 1.08 +/- 0.02 L/min/SaO2% at basal condition and 0.53 +/- 0.07 L/min/SaO2% after 1 month of treatment, p = 0.008) [mean +/- SD], but not in patients treated with sham nCPAP (slope, 0.83 +/- 0.09 L/min/SaO2% and 0.85 +/- 0.19 L/min/SaO2% at basal condition and after 1 month, respectively). The normoxic hypercapnic ventilatory response remained unchanged after 1 month in both groups. No changes in ventilatory response to either hypoxia or hypercapnia were observed after a single night of nCPAP treatment. CONCLUSION: The ventilatory response to hypoxia is reduced during regular treatment, but not after short-term treatment, with nCPAP. Readjusted peripheral oxygen chemosensitivity during nCPAP treatment may be a side effect of both reduced sympathetic activity and increased baroreflex activity, or a possible continuous positive airway pressure-related mechanism leading to a reduced activation of autonomic nervous system per se.

Autonomic Nervous System↗
PubMed2005

Slow breathing improves arterial baroreflex sensitivity and decreases blood pressure in essential hypertension.

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4+/-1.9 years) and in 26 controls (52.3+/-1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7+/-3.7 to 141.1+/-4 mm Hg, P<0.05; and from 82.7+/-3 to 77.8+/-3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8+/-3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8+/-0.7 to 10.3+/-2.0 ms/mm Hg; P<0.01) and controls (from 10.9+/-1.0 to 16.0+/-1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

Arteries↗
PubMed2005

Frequency-dependent baroreflex control of blood pressure and heart rate during physical exercise.

BACKGROUND: It is widely recognised that during exercise vagal heart rate control is markedly impaired but blood pressure control may or may not be retained. We hypothesised that this uncertainty arose from the differing responses of the vagus (fast) and sympathetic (slow) arms of the autonomic effectors, and to differing sympatho-vagal balance at different exercise intensities. METHODS AND RESULTS: We studied 12 normals at rest, during moderate (50% maximal heart rate) and submaximal (80% maximal heart rate) exercise. The carotid baroreceptors were stimulated by sinusoidal neck suction at the frequency of the spontaneous high- (during moderate exercise) and low-frequency (during submaximal) fluctuations in heart period and blood pressure. The increases in these oscillations induced by neck suction were measured by autoregressive spectral analysis. At rest neck stimulation increased variability at low frequency (RR: from 6.99+/-0.24 to 8.87+/-0.18 ln-ms2; systolic pressure: from 3.05+/-1.7 to 4.09+/-0.17 ln-mm Hg2) and high frequency (RR: from 4.67+/-0.25 to 6.79+/-0.31 ln-ms2; systolic pressure: from 1.93+/-0.2 to 2.67+/-0.125 ln-mm Hg2) (all p<0.001). During submaximal exercise RR variability decreased but systolic pressure variability rose (p<0.01 vs rest); during submaximal exercise low-frequency neck stimulation increased the low-frequency fluctuations in blood pressure (2.35+/-0.51 to 4.25+/-0.38 ln-mm Hg2, p<0.05) and RR. Conversely, neck suction at high frequency was ineffective on systolic pressure, and had only minor effects on RR interval during moderate exercise. CONCLUSION: During exercise baroreflex control is active on blood pressure, but the efferent response on blood pressure and heart rate is only detected during low frequency stimulation, indicating a frequency-dependent effect.

Adult↗
PubMed2005

Interaction between central-peripheral chemoreflexes and cerebro-cardiovascular control.

We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO(2)), and to normoxic hypercapnia. Oxygen saturation (SaO(2)), end-tidal CO(2) (et-CO(2)), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O(2): -0.33 +/- 0.05, -0.74 +/- 0.02 and -1.59 +/- 0.3, p < 0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO(2), whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO(2). We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.

Adult↗
PubMed2005

Consensus statement on chronic and subacute high altitude diseases.

This is an international consensus statement of an ad hoc committee formed by the International Society for Mountain Medicine (ISMM) at the VI World Congress on Mountain Medicine and High Altitude Physiology (Xining, China; 2004) and represents the committee's interpretation of the current knowledge with regard to the most common chronic and subacute high altitude diseases. It has been developed by medical and scientific authorities from the committee experienced in the recognition and prevention of high altitude diseases and is based mainly on published, peer-reviewed articles. It is intended to include all legitimate criteria for choosing to use a specific method or procedure to diagnose or manage high altitude diseases. However, the ISMM recognizes that specific patient care decisions depend on the different geographic circumstances involved in the development of each chronic high altitude disease. These guidelines are established to inform the medical services on site who are directed to solve high altitude health problems about the definition, diagnosis, treatment, and prevention of the most common chronic high altitude diseases. The health problems associated with life at high altitude are well documented, but health policies and procedures often do not reflect current state-of-the-art knowledge. Most of the cases of high altitude diseases are preventable if on-site personnel identify the condition and implement appropriate care.

Acclimatization↗
PubMed2003

Effects of unilateral and bilateral carotid baroreflex stimulation on cardiac and neural sympathetic discharge oscillatory patterns.

BACKGROUND: Left and right carotid baroreflex afferents participate in generating the spontaneous variability of heart rate (HR), arterial pressure (AP), and muscle sympathetic nerve activity (MSNA), but the relative contribution of each side is unclear. Pathophysiological conditions unilaterally affecting carotid baroreceptor function might result in abnormal changes of HR, AP, and MSNA variability, thus markedly affecting prognosis. We tested the hypothesis that unilateral carotid baroreceptor perturbation might differentially affect HR, AP, and MSNA variability compared with stimulation of the opposite side. METHODS AND RESULTS: In 12 healthy volunteers, 4 sinusoidal neck suction procedures (0.1 Hz, from 0 to -50 mm Hg) were applied at the right, left, and combined right and left sides of the neck, in concordance or with phase opposition. Respiration was controlled at 0.25 Hz. Power spectrum analysis assessed the changes in the 0.1-Hz oscillatory component of the R-R interval, systolic AP (SAP), and MSNA variability induced by rhythmic baroreceptor stimulation. Mean R-R interval, SAP, and MSNA were unchanged during all procedures. The increase of the 0.1-Hz component of R-R and SAP variability during right and combined right and left carotid baroreceptor stimulation was greater than the changes induced by left-sided stimulation. The increase in the 0.1-Hz oscillatory component of MSNA variability was similar during all neck suction procedures. CONCLUSIONS: Right carotid baroreflex loading was as efficient as bilateral stimulation and more effective than left carotid suction in modulating R-R and SAP variability. There was no asymmetry in neural sympathetic discharge responses after single-sided carotid baroreceptor stimulation.

Adult↗
PubMed2003

Gene expression in the Andes; relevance to neurology at sea level.

Chronic mountain sickness (CMS), a maladaptation syndrome to chronic hypoxia, occurs in the Andes. Gene expression differences in Andeans could explain adaptation and maladaptation to hypoxia, both of which are relevant to neurology at sea level. Expression of genes responsive to cellular oxygen concentration, hypoxia-inducible factor-1alpha (HIF-1alpha), three splicing variants of vascular endothelial growth factor (VEGF) and von Hippel-Lindau protein (pVHL) was measured by reverse transcription polymerase chain reaction (RT-PCR) in 12 Cerro de Pasco (CP) (altitude 4338 m) natives and 15 CMS patients in CP. Thirteen high altitude natives living in Lima and five Lima natives were sea level controls. A CMS score (CMS-sc) was assigned clinically. Expression was related to the clinical assessment. High expression of HIF-1alpha and VEGF-121 was found in CMS (P<0.001). Samples from CP had higher expression than those from Lima (P<0.001). Expression of HIF-1alpha and VEGF-121 was related to age (P<0.001); adjusting for age did not abolish the group effect. Higher CMS-sc was related to expression independent of age (P<0.001). VEGF-165 and -189 were expressed only in CMS. Birth altitude had no effect on gene expression. pVHL was not quantifiable.HIF-1alpha and VEGF-121 participate in adaptation to hypoxia. The high levels may explain blood vessel proliferation in Andeans and hold lessons for patients at sea level. VEGF-165 expression suggests that it contributes to preservation of neuronal function in human chronic hypoxia. VHL mutations may mark those destined to develop neural crest tumors which are common in the Andes.

Adult↗
PubMed2003

Ventilation, autonomic function, sleep and erythropoietin. Chronic mountain sickness of Andean natives.

Polycythemia is one of the key factors involved in the chronic mountain sickness syndrome, a condition frequent in Andean natives but whose causes still remain unclear. In theory, polycythemia may be secondary to abnormalities in ventilation, occurring during day or night (e.g. due to sleep abnormalities) stimulating excessive erythropoietin (Epo) production, or else it may result from either autogenous production, or from co-factors like cobalt. To assess the importance of these points, we studied subjects with or without polycythemia, born and living in Cerro de Pasco (Peru, 4330m asl, CP) and evaluated the relationship between Epo and respiratory variables both in CP and sea level. We also assessed the relationship between sleep abnormalities and the circadian rhythm of Epo. Polycythemic subjects showed higher Epo in all conditions, lower SaO2 and hypoxic ventilatory response, higher physiological dead space and higher CO2, suggesting ventilatory inefficiency. Epo levels could be highly modified by the level of oxygenation, and were related to similar directional changes in SaO2. Cobalt levels were normal in all subjects and correlated poorly with hematologic variables. The diurnal variations in Epo were grossly abnormal in polycythemic subjects, with complete loss of the circadian rhythm. These abnormalities correlated with the levels of hypoxemia during the night, but not with sleep abnormalities, which were only minor even in polycythemic subjects. The increased Epo production is mainly related to a greater ventilatory inefficiency, and not to altered sensitivity to hypoxia, cobalt or sleep abnormalities. Improving oxygenation can represent a possible therapeutic option for this syndrome.

Altitude Sickness↗
PubMed2002

Autonomic modulation of heart rate during obstructive versus central apneas in patients with sleep-disordered breathing.

Sleep-disordered breathing is associated with an altered sympathovagal balance determined by the nocturnal cyclic alternating of apneas and hyperventilation. The aim of this study was to determine whether the autonomic modulation of heart rate during obstructive apneas (OA) and central apneas (CA) in patients with sleep-disordered breathing is different. Therefore, by using the time-varying Wigner-Ville transform spectral analysis we described, in 17 patients, the time course of the low-frequency (LF) and the high-frequency (HF) components of the interbeat interval (R-R interval) reflecting, at large, respectively, the sympathetic and the parasympathetic modulation, during OA (n = 185) and CA (n = 51) and during the postapneic hyperventilation. In both types of apneas we found cyclic lengthening/shortening in R-R interval, during apneas/postapneic hyperventilation, respectively, with more marked bradycardia during OA (R-R: 1,011 +/- 23 versus 893 +/- 30 ms2, p < 0.01). In OA the HF oscillations decreased from the apnea to the postapneic hyperventilation (from 1,964 +/- 244 to 387 +/- 98 ms2, p < 0.0001), whereas the LF oscillations increased (from 2,649 +/- 230 to 9,820 +/- 716 ms2, p < 0.0001). Conversely, in CA the HF oscillations increased from the apnea to the postapneic hyperventilation (from 452 +/- 177 to 1,485 +/- 406 ms2, p < 0.0001), whereas the LF component remained unchanged. These results show markedly different autonomic alterations during and after OA versus CA, suggesting a surge in sympathetic modulation after the obstructive episodes.

Aged↗
PubMed2002

Respiratory and cerebrovascular responses to hypoxia and hypercapnia in familial dysautonomia.

Although cardiorespiratory complications contribute to the high morbidity/mortality of familial dysautonomia (FD), the mechanisms remain unclear. We evaluated respiratory, cardiovascular, and cerebrovascular control by monitoring ventilation, end-tidal carbon dioxide (CO2-et), oxygen saturation, RR interval, blood pressure (BP), and midcerebral artery flow velocity (MCFV) during progressive isocapnic hypoxia, progressive hyperoxic hypercapnia, and during recovery from moderate hyperventilation (to simulate changes leading to respiratory arrest) in 22 subjects with FD and 23 matched control subjects. Subjects with FD had normal ventilation, higher CO2-et, lower oxygen saturation, lower RR interval, and higher BP. MCFV was also higher but depended on the higher baseline CO2-et. In the FD group, whereas hyperoxic hypercapnia induced normal cardiovascular and ventilatory responses, progressive hypoxia resulted in blunted increases in ventilation, paradoxical decreases in RR interval and BP, and lack of MCFV increase. Hyperventilation induced a longer hypocapnia-induced apneic period (51.5 +/- 9.9 versus 11.2 +/- 5.5 seconds, p < 0.008) with profound desaturation (to 75.8 +/- 3.5%), marked BP decrease, and RR interval increase. Subjects with FD develop central depression in response to even moderate hypoxia with lack of expected change in cerebral circulation, leading to hypotension, bradycardia, hypoventilation, and potentially respiratory arrest. Higher resting BP delays occurrence of syncope during hypoxia. Therapeutic measures preventing hypoxia/hypocapnia may correct cardiovascular accidents in patients with FD.

Adaptation, Physiological↗
PubMed2002

Slow breathing increases arterial baroreflex sensitivity in patients with chronic heart failure.

BACKGROUND: It is well established that a depressed baroreflex sensitivity may adversely influence the prognosis in patients with chronic heart failure (CHF) and in those with previous myocardial infarction. METHODS AND RESULTS: We tested whether a slow breathing rate (6 breaths/min) could modify the baroreflex sensitivity in 81 patients with stable (2 weeks) CHF (age, 58+/-1 years; NYHA classes I [6 patients], II [33], III [27], and IV [15]) and in 21 controls. Slow breathing induced highly significant increases in baroreflex sensitivity, both in controls (from 9.4+/-0.7 to 13.8+/-1.0 ms/mm Hg, P<0.0025) and in CHF patients (from 5.0+/-0.3 to 6.1+/-0.5 ms/mm Hg, P<0.0025), which correlated with the value obtained during spontaneous breathing (r=+0.202, P=0.047). In addition, systolic and diastolic blood pressure decreased in CHF patients (systolic, from 117+/-3 to 110+/-4 mm Hg, P=0.009; diastolic, from 62+/-1 to 59+/-1 mm Hg, P=0.02). CONCLUSIONS: These data suggest that in patients with CHF, slow breathing, in addition to improving oxygen saturation and exercise tolerance as has been previously shown, may be beneficial by increasing baroreflex sensitivity.

Arteries↗
PubMed2002

Sinusoidal neck suction for evaluation of baroreflex sensitivity during desflurane and sevoflurane anesthesia.

UNLABELLED: Sevoflurane and desflurane modulate autonomic nervous activity by different mechanisms. We tested the hypothesis that these anesthetics also exhibit different effects on short-term baroreflex regulation of arterial blood pressure. Forty ASA physical status I patients, aged 20 to 42 yr, were randomly assigned to receive either 1.0 minimum alveolar anesthetic concentration of sevoflurane or desflurane for the maintenance of anesthesia. Patients were studied during awake conditions and 20 min after the anesthesia induction using sinusoidal neck suction at 0.2 Hz (baroreflex response mediated mainly by vagal activity) and 0.1 Hz (baroreflex response mediated by vagal and sympathetic activity), whereas respiratory frequency was fixed at 0.25 Hz. RR interval and arterial blood pressure responses were evaluated by power spectral analysis and complex transfer function analysis. Sevoflurane and desflurane did not disturb the linear relationship between baroreceptor stimulation and effector response, expressed as squared coherence of signals, i.e., the equivalent of the correlation coefficient of power spectra. Sevoflurane and desflurane depressed the response of the heart rate to neck suction in a similar way without affecting the time delay between baroreceptor stimulation and vagal-mediated cardiac response. The gain of the transfer function between neck suction and oscillation in arterial blood pressure at 0.1 Hz decreased with sevoflurane and desflurane to comparable values. Both anesthetics increased the delay of systolic blood pressure response to baroreceptor stimulation from approximately 3.5 to 4.3 s. Baroreflex-mediated short-term control of arterial blood pressure is similar between desflurane and sevoflurane during steady-state conditions. IMPLICATIONS: Despite exhibiting different effects on autonomic activity, sevoflurane and desflurane depress the baroreflex-mediated short-term control of heart rate and blood pressure in a similar manner.

Adult↗