Pulse arrival time: Measurement and clinical applications

Pulse arrival time is the time elapsed between the R-wave of electrocardiogram and systolic peak in peripheral pulse obtained by any of the plethysmographic methods. Similarly, differential pulse arrival time, also known as pulse transit time, is the time elapsed between systolic peaks of proximal and distal peripheral pulse recordings in an extremity. Distance between the proximal and distal site in the extremity (in meters) divided by differential pulse arrival time (in seconds) gives arterial pulse wave velocity in the limb segment. Differential pulse arrival time has been used to discriminate between an aortic or arterial block from generalized atherosclerosis in aortic and arterial occlusive diseases for nearly four decades. All along there have been efforts to monitor beat-to-beat blood pressure with the help of these time intervals and other pulse parameters. Encouraging correlation has been observed with that obtained by Finapres. Recently pulse arrival time has been explored for the prompt detection of sudden hypertensive episodes during laryngeal microsurgery, for detection of mental stress, monitoring of baroreflex sensitivity, and real-time monitoring of blood pressure. This paper briefly describes the measurement technique of pulse arrival time and an overview of its clinical applications.

Patterns of renal and splanchnic sympathetic vasomotor activity in an animal model of survival to experimental sepsis

Sepsis causes long-term disability, such as immune dysfunction, neuropsychological disorders, persistent inflammation, catabolism, and immunosuppression, leading to a high risk of death in survivors, although the contributing factors of mortality are unknown. The purpose of this experimental study in rats was to examine renal (rSNA) and splanchnic (sSNA) sympathetic nerve activity, as well as baroreflex sensitivity, in acute and chronic post-sepsis periods. The rats were divided into two groups: control group with naïve Wistar rats and sepsis group with 2-mL intravenous inoculation of Escherichia coli at 108 CFU/mL. Basal mean arterial pressure, heart rate, rSNA, sSNA, and baroreflex sensitivity were evaluated in all groups at the acute (6 h) and chronic periods (1 and 3 months). Basal rSNA and sSNA were significantly reduced in the surviving rats, as was their baroreflex sensitivity, for both pressor and hypotensive responses, and this effect lasted for up to 3 months. A single episode of sepsis in rats was enough to induce long-term alterations in renal and splanchnic sympathetic vasomotor nerve activity, representing a possible systemic event that needs to be elucidated. These findings showed that post-sepsis impairment of sympathetic vasomotor response may be one of the critical components in the inability of sepsis survivors to respond effectively to new etiological illness factors, thereby increasing their risk of post-sepsis morbidity.

Naringin and trimetazidine improve baroreflex sensitivity and nucleus tractus solitarius electrical activity in renal ischemia-reperfusion injury / Naringin and trimetazidine improve baroreflex sensitivity and nucleus tractus solitarius electrical activity in renal ischemia-reperfusion injury

Resumo Fundamento: O núcleo do trato solitário (NTS) é uma área do cérebro que desempenha um papel fundamental na regulação renal e cardiovascular através dos impulsos dos barorreceptores. Objetivos: O objetivo deste estudo foi avaliar o efeito da Naringina (NAR) e trimetazidina (TMZ), isoladamente e combinadas, na atividade elétrica do NTS e na sensibilidade barorreflexa (SBR) na lesão de isquemia e reperfusão (I/R) renal. Métodos: Foram utilizados quarenta ratos machos Sprague-Dawley (200-250 g), alocados em 5 grupos com 8 ratos cada. Grupos: 1) Sham; 2) I/R; 3) TMZ 5 mg/kg; 4) NAR 100 mg/kg; e 5) TMZ5 + NAR100. A veia femoral esquerda foi canulada para infundir a solução salina ou droga e avaliar a SBR. A I/R foi induzida por oclusão dos pedículos renais por 45 min, seguida de reperfusão de 4 horas. O eletroencefalograma local do NTS foi registrado antes, durante a isquemia e durante a reperfusão. A fenilefrina foi injetada por via intravenosa para avaliar a SBR ao final do tempo de reperfusão. Os dados foram analisados por ANOVA de duas vias com medidas repetidas seguida pelo teste post hoc de Tukey. Um valor de p<0,05 foi considerado como significativo. Resultados: As ondas elétricas do NTS não se alteraram durante o tempo de isquemia, mas diminuíram significativamente durante todos os tempos de reperfusão. A atividade elétrica do NTS e a SBR foram reduzidas drasticamente em ratos com lesão I/R; no entanto, a administração de NAR e TMZ, isoladamente e combinadas, melhorou significativamente essas alterações em ratos com lesão I/R. Conclusões: Os resultados mostraram que a lesão de I/R leva à redução da atividade elétrica da SBR e do NTS, e pode haver uma ligação entre a I/R e a diminuição da SBR. Além disso, a NAR e a TMZ são agentes promissores para tratar complicações de I/R.

Abstract Background: Nucleus tractus solitarius (NTS) is a brain area that plays a key role in kidney and cardiovascular regulation via baroreceptors impulses. Objectives: The aim of this study was to evaluate the effect of naringin (NAR) and trimetazidine (TMZ) alone and their combination on NTS electrical activity and baroreceptor sensitivity (BRS) in renal ischemia- reperfusion (I/R) injury. Methods: Forty male Sprague-Dawley rats (200- 250 g) were allocated into 5 groups with 8 in each. 1) Sham; 2) I/R; 3) TMZ 5 mg/kg; 4) NAR 100 mg/kg; and 5) TMZ5+ NAR100. The left femoral vein was cannulated to infuse saline solution or drug and the BRS was evaluated. I/R was induced by occlusion of renal pedicles for 45 min, followed by 4 hours of reperfusion. The NTS local electroencephalogram (EEG) was recorded before, during ischemia and throughout the reperfusion. Phenylephrine was injected intravenously to evaluate BRS at the end of reperfusion time. The data were analyzed by two-way repeated measurement ANOVA followed by Tukey's post hoc test. A p-value <0.05 was considered significant. Results: NTS electrical waves did not change during ischemia time, while they significantly decreased during the entire reperfusion time. NTS electrical activity and BRS dramatically reduced in rats with I/R injury; however, administration of NAR, TMZ alone or their combination significantly improved these changes in rats with I/R injury. Conclusions: The results showed that I/R injury leads to reduced BRS and NTS electrical activity and there may be an association between I/R and decreased BRS. In addition, NAR and TMZ are promising agents to treat I/R complications.

Multicomponent exercise training in cardiovascular complexity in prefrail older adults: a randomized blinded clinical pilot study

The aim of this study was to investigate the effects of multicomponent training on baroreflex sensitivity (BRS) and heart rate (HR) complexity of prefrail older adults. Twenty-one prefrail community-dwelling older adults were randomized and divided into multicomponent training intervention group (MulTI) and control group (CG). MulTI performed multicomponent exercise training over 16 weeks and CG was oriented to follow their own daily activities. The RR interval (RRi) and blood pressure (BP) series were recorded for 15 min in supine and 15 min in orthostatic positions, and calculation of BRS (phase, coherence, and gain) and HR complexity (sample entropy) were performed. A linear mixed model was applied for group, assessments, and their interaction effects in supine position. The same test was used to assess the active postural maneuver and it was applied separately to each group considering assessments (baseline and post-intervention) and positions (supine and orthostatic). The significance level established was 5%. Cardiovascular control was impaired in prefrail older adults in supine position. Significant interactions were not observed between groups or assessments in terms of cardiovascular parameters. A 16-week multicomponent exercise training did not improve HR complexity or BRS in supine rest or in active postural maneuver in prefrail older adults.

Effects of exercise training on autonomic modulation and mood symptoms in patients with obstructive sleep apnea

We evaluated the effects of exercise training (ET) on the profile of mood states (POMS), heart rate variability, spontaneous baroreflex sensitivity (BRS), and sleep disturbance severity in patients with obstructive sleep apnea (OSA). Forty-four patients were randomized into 2 groups, 18 patients completed the untrained period and 16 patients completed the exercise training (ET). Beat-to-beat heart rate and blood pressure were simultaneously collected for 5 min at rest. Heart rate variability (RR interval) was assessed in time domain and frequency domain (FFT spectral analysis). BRS was analyzed with the sequence method, and POMS was analyzed across the 6 categories (tension, depression, hostility, vigor, fatigue, and confusion). ET consisted of 3 weekly sessions of aerobic exercise, local strengthening, and stretching exercises (72 sessions, achieved in 40±3.9 weeks). Baseline parameters were similar between groups. The comparisons between groups showed that the changes in apnea-hypopnea index, arousal index, and O2 desaturation in the exercise group were significantly greater than in the untrained group (P<0.05). The heart rate variability and BRS were significantly higher in the exercise group compared with the untrained group (P<0.05). ET increased peak oxygen uptake (P<0.05) and reduced POMS fatigue (P<0.05). A positive correlation (r=0.60, P<0.02) occurred between changes in the fatigue item and OSA severity. ET improved heart rate variability, BRS, fatigue, and sleep parameters in patients with OSA. These effects were associated with improved sleep parameters, fatigue, and cardiac autonomic modulation, with ET being a possible protective factor against the deleterious effects of hypoxia on these components in patients with OSA.

Research progress on ion channels and receptors in nodose ganglion neurons involved in blood pressure regulation / 药学学报

Hypertension is the most common cardiovascular disease. In recent years, reduced baroreceptor activity has been suggested as a main cause of hypertension. The cell body of the primary afferent nerve of the baroreceptor is located in the nodose ganglion (NG). The ion channels and receptors in the NG can affect baroreceptor sensitivity and neuronal excitability, thus regulating blood pressure. This review focuses on recent research progress on ion channels, receptors and other proteins in NG neurons that are involved in modulating the sensitivity of the baroreceptor reflex to regulate blood pressure.

Baroreflex sensitivity in frailty syndrome

Frailty is related to a decrease in the physiological reserves, which causes difficulties in maintaining homeostasis. An example of physiological mechanisms for cardiovascular homeostasis is the baroreflex. The aim of this study was to compare baroreflex among frail, prefrail, and nonfrail individuals, in supine and orthostatic positions. Community-dwelling older adults were evaluated and categorized into frail, prefrail, or nonfrail groups, according to frailty phenotype. The RR interval (RRi) and systolic blood pressure (SBP) series were recorded for 15 min in the supine and 15 min in the orthostatic positions. Mean and variance of RRi and SBP, and baroreflex evaluated by phase, gain (α), and coherence (K2) were determined. A two-way repeated measures ANOVA, with Tukey's post hoc, was applied for group, position, and their interaction effects. The significance level established was 5%. Prefrail and frail participants did not present a significant decrease in mean values of RRi after postural challenge (893.43 to 834.20 ms and 925.99 to 857.98 ms, respectively). Frail participants showed a reduction in RRi variance in supine to orthostatic (852.04 to 232.37 ms2). Prefrail and frail participants showed a decrease in K2 after postural change (0.69 to 0.52 and 0.54 to 0.34, respectively). Frail participants exhibited lower values of K2 (0.34) compared to nonfrail and prefrail participants (0.61 and 0.52, respectively). Baroreflex indicated the presence of decoupling between heart period and SBP in frail and prefrail. Thus, reduced K2 might be a marker of the frailty process.

Cellular and Molecular Mechanisms Underlying Arterial Baroreceptor Remodeling in Cardiovascular Diseases and Diabetes / 神经科学通报·英文版

Clinical trials and animal experimental studies have demonstrated an association of arterial baroreflex impairment with the prognosis and mortality of cardiovascular diseases and diabetes. As a primary part of the arterial baroreflex arc, the pressure sensitivity of arterial baroreceptors is blunted and involved in arterial baroreflex dysfunction in cardiovascular diseases and diabetes. Changes in the arterial vascular walls, mechanosensitive ion channels, and voltage-gated ion channels contribute to the attenuation of arterial baroreceptor sensitivity. Some endogenous substances (such as angiotensin II and superoxide anion) can modulate these morphological and functional alterations through intracellular signaling pathways in impaired arterial baroreceptors. Arterial baroreceptors can be considered as a potential therapeutic target to improve the prognosis of patients with cardiovascular diseases and diabetes.

Anti-Hypertensive Action of Fenofibrate via UCP2 Upregulation Mediated by PPAR Activation in Baroreflex Afferent Pathway / 神经科学通报·英文版

Fenofibrate, an agonist for peroxisome proliferator-activated receptor alpha (PPAR-α), lowers blood pressure, but whether this action is mediated via baroreflex afferents has not been elucidated. In this study, the distribution of PPAR-α and PPAR-γ was assessed in the nodose ganglion (NG) and the nucleus of the solitary tract (NTS). Hypertension induced by drinking high fructose (HFD) was reduced, along with complete restoration of impaired baroreceptor sensitivity, by chronic treatment with fenofibrate. The molecular data also showed that both PPAR-α and PPAR-γ were dramatically up-regulated in the NG and NTS of the HFD group. Expression of the downstream signaling molecule of PPAR-α, the mitochondrial uncoupling protein 2 (UCP2), was up-regulated in the baroreflex afferent pathway under similar experimental conditions, along with amelioration of reduced superoxide dismutase activity and increased superoxide in HFD rats. These results suggest that chronic treatment with fenofibrate plays a crucial role in the neural control of blood pressure by improving baroreflex afferent function due at least partially to PPAR-mediated up-regulation of UCP2 expression and reduction of oxidative stress.

Baroreflex Control of Heart Rate in Mice Overexpressing Human SOD1: Functional Changes in Central and Vagal Efferent Components / 神经科学通报·英文版

Excessive reactive oxygen species (ROS) (such as the superoxide radical) are commonly associated with cardiac autonomic dysfunctions. Though superoxide dismutase 1 (SOD1) overexpression may protect against ROS damage to the autonomic nervous system, superoxide radical reduction may change normal physiological functions. Previously, we demonstrated that human SOD1 (hSOD1) overexpression does not change baroreflex bradycardia and tachycardia but rather increases aortic depressor nerve activity in response to arterial pressure changes in C57B6SJL-Tg (SOD1)2 Gur/J mice. Since the baroreflex arc includes afferent, central, and efferent components, the objective of this study was to determine whether hSOD1 overexpression alters the central and vagal efferent mediation of heart rate (HR) responses. Our data indicate that SOD1 overexpression decreased the HR responses to vagal efferent nerve stimulation but did not change the HR responses to aortic depressor nerve (ADN) stimulation. Along with the previous study, we suggest that SOD1 overexpression preserves normal baroreflex function but may differentially alter the functions of the ADN, vagal efferents, and central components. While SOD1 overexpression likely enhanced ADN function and the central mediation of bradycardia, it decreased vagal efferent control of HR.

Role of adenosine A1 receptor within nucleus tractus solitarii in dexmedetomidine-induced increase in baroreflex sensitivity in rats / 中华麻醉学杂志

Objective To evaluate the role of A1 adenosine receptor ( A1 AR) within the nucleus tractus solitarii ( NTS ) in dexmedetomidine-induced increase in baroreflex sensitivity ( BRS ) in rats. Methods Thirty-two clean-grade healthy male Sprague-Dawley rats, weighing 240-280 g, were divided in-to 4 groups ( n=8 each) using a random number table method: control group ( group C) , solvent control group ( group S) , dexmedetomidine group ( group D) , and dexmedetomidine plus 8-cyclopentyl-1,3-diprop-ylxanthine (DPCPX, a highly selective A1AR blocker) group (group DD). After the rats were anesthe-tized, 1 μl drug liquid was injected into the right NTS with a brain stereotaxic apparatus. Oneμl normal sa-line was injected into the right NTS in C and D groups, 1 μl dimethyl sulfoxide in group S, and 1 μl DPCPX in group DD. After catheters were implanted into the femoral vein, dexmedetomidine was intrave-nously infused as a bolus of 100μg/kg over 15 min followed by an infusion of 50μg·kg-1 ·h-1 for 105 min in D and DD groups. The equal volume of normal saline was given instead of dexmedetomidine in C and S groups. BRS was measured using phenylephrine immediately before intravenous infusion (T0) and at 60 and 120 min after beginning of infusion ( T1,2 ) . Results Compared with C and S groups, the BRS was signifi-cantly increased at T1,2 in D and DD groups ( P＜0. 05) . Compared with group D, the BRS was significantly decreased at T1,2 in group DD ( P＜0. 05) . Conclusion A1 AR within the NTS is involved in dexmedetomi-dine-induced increase in BRS in rats.

Impaired baroreflex sensitivity and increased systolic blood pressure variability in chronic post-ischemic stroke

OBJECTIVES: Acute post-stroke patients present cardiovascular autonomic dysfunction, which manifests as lower heart rate variability and impaired baroreflex sensitivity. However, few studies performed to date have evaluated cardiovascular autonomic function in chronic post-stroke patients. The aim of this study was to evaluate cardiovascular autonomic modulation in chronic post-ischemic stroke patients. METHODS: The seventeen enrolled subjects were divided into a stroke group (SG, n=10, 5±1 years after stroke) and a control group (CG, n=7). Non-invasive curves for blood pressure were continuously recorded (Finometer®) for 15 minutes while the subject was in a supine position. Heart rate variability and blood pressure variability were analyzed in the time and frequency domains. RESULTS: No differences were observed in systolic and diastolic pressure and heart rate between post-stroke patients and healthy individuals. The SG group had lower indexes for heart rate variability in the time domain (standard deviation of normal to normal R-R intervals, SDNN; variance of normal to normal R-R intervals, VarNN; and root mean square differences of successive R-R intervals, RMSSD) and a lower high-frequency band for heart rate variability than was observed in the CG. Systolic blood pressure variability and the low-frequency band for systolic pressure were higher in post-stroke patients, while the alpha index was lower in the SG than in the CG. CONCLUSION: After ischemic stroke, affected patients present chronically reduced heart rate variability, impaired cardiac vagal modulation, increased systolic blood pressure variability and higher sympathetic vascular modulation along with impaired baroreflex sensitivity, which can increase the risk of cardiovascular events, despite adequate blood pressure control.

Resting spontaneous baroreflex sensitivity and cardiac autonomic control in anabolic androgenic steroid users

OBJECTIVES: Misuse of anabolic androgenic steroids in athletes is a strategy used to enhance strength and skeletal muscle hypertrophy. However, its abuse leads to an imbalance in muscle sympathetic nerve activity, increased vascular resistance, and increased blood pressure. However, the mechanisms underlying these alterations are still unknown. Therefore, we tested whether anabolic androgenic steroids could impair resting baroreflex sensitivity and cardiac sympathovagal control. In addition, we evaluate pulse wave velocity to ascertain the arterial stiffness of large vessels. METHODS: Fourteen male anabolic androgenic steroid users and 12 nonusers were studied. Heart rate, blood pressure, and respiratory rate were recorded. Baroreflex sensitivity was estimated by the sequence method, and cardiac autonomic control by analysis of the R-R interval. Pulse wave velocity was measured using a noninvasive automatic device. RESULTS: Mean spontaneous baroreflex sensitivity, baroreflex sensitivity to activation of the baroreceptors, and baroreflex sensitivity to deactivation of the baroreceptors were significantly lower in users than in nonusers. In the spectral analysis of heart rate variability, high frequency activity was lower, while low frequency activity was higher in users than in nonusers. Moreover, the sympathovagal balance was higher in users. Users showed higher pulse wave velocity than nonusers showing arterial stiffness of large vessels. Single linear regression analysis showed significant correlations between mean blood pressure and baroreflex sensitivity and pulse wave velocity. CONCLUSIONS: Our results provide evidence for lower baroreflex sensitivity and sympathovagal imbalance in anabolic androgenic steroid users. Moreover, anabolic androgenic steroid users showed arterial stiffness. Together, these alterations might be the mechanisms triggering the increased blood pressure in this population.

Exercise training attenuates hypertension progression via activation of central ACE2-Ang(1-7)-Mas axis in prehypertensive rats / 中国病理生理杂志

AIM:To investigate the effects of exercise training on the progression from prehypertension to hy -pertension,blood pressure regulation and the angiotensin-converting enzyme 2(ACE2)-angiotensin(Ang)(1-7)-MAS axis activation in cardiovascular centers ,and to elucidate the central mechanisms of exercise training postponing hyperten -sion progression.METHODS:The male spontaneously hypertensive rats(SHR;n=20,5 weeks old)and normotensive Wistar Kyoto(WKY)rats(n=20)were randomly assigned to sedentary(Sed)group and exercise training(ExT)group. The trained rats run on a treadmill in moderate-intensity for 20 weeks.Systolic blood pressure(SBP)was measured by tail-cuff method.The baroreflex sensitivity(BRS)was assessed by intravenous injection of phenylephrine.The expression of ACE2 and MAS receptor at mRNA and protein levels in baroreflex centers were determined by real-time PCR and Western blot,respectively.Alterations of BRS were evaluated before and after intracerebroventricular injection of MAS receptor ago -nist Ang(1-7)and its antagonist A779,respectively.RESULTS:Compared with SHR +Sed group,exercise training since prehypertension significantly postponed the development of hypertension ,delayed the hypertension progression ,and decreased SBP in both SHR and WKY rats(P<0.05).Exercise training enhanced blood pressure regulation and improved the BRS in SHR(P<0.01).The expression of ACE2 and MAS receptor at mRNA and protein levels in the baroreflex cen-ters(rostral ventrolateral medulla ,nucleus tract solitarius and paraventricular nucleus )were up-regulated in SHR +ExT group(P<0.05).Central administration of A779 abolished the benefits of exercise-induced improvement of BRS in SHR +ExT group(P<0.01).In contrast,Ang(1-7)improved the BRS in both SHR +Sed group and SHR +ExT group(P<0.05).CONCLUSION:Exercise training postpones hypertension progression and improves blood pressure regula -tion,which may be associated with the activation of central ACE 2-Ang(1-7)-Mas axis.

The Effect of Physical Resistance Training on Baroreflex Sensitivity of Hypertensive Rats / Efeito do Treinamento Físico Resistido na Sensibilidade Barorreflexa de Ratos Hipertensos

Abstract Background: Baroreceptors act as regulators of blood pressure (BP); however, its sensitivity is impaired in hypertensive patients. Among the recommendations for BP reduction, exercise training has become an important adjuvant therapy in this population. However, there are many doubts about the effects of resistance exercise training in this population. Objective: To evaluate the effect of resistance exercise training on BP and baroreceptor sensitivity in spontaneously hypertensive rats (SHR). Method: Rats SHR (n = 16) and Wistar (n = 16) at 8 weeks of age, at the beginning of the experiment, were randomly divided into 4 groups: sedentary control (CS, n = 8); trained control (CT, n = 8); sedentary SHR (HS, n = 8) and trained SHR (HT, n = 8). Resistance exercise training was performed in a stairmaster-type equipment (1.1 × 0.18 m, 2 cm between the steps, 80° incline) with weights attached to their tails, (5 days/week, 8 weeks). Baroreceptor reflex control of heart rate (HR) was tested by loading/unloading of baroreceptors with phenylephrine and sodium nitroprusside. Results: Resistance exercise training increased the soleus muscle mass in SHR when compared to HS (HS 0.027 ± 0.002 g/mm and HT 0.056 ± 0.003 g/mm). Resistance exercise training did not alter BP. On the other hand, in relation to baroreflex sensitivity, bradycardic response was improved in the TH group when compared to HS (HS -1.3 ± 0.1 bpm/mmHg and HT -2.6 ± 0.2 bpm/mmHg) although tachycardia response was not altered by resistance exercise (CS -3.3 ± 0.2 bpm/mmHg, CT -3.3 ± 0.1 bpm/mmHg, HS -1.47 ± 0.06 bpm/mmHg and HT -1.6 ± 0.1 bpm/mmHg). Conclusion: Resistance exercise training was able to promote improvements on baroreflex sensitivity of SHR rats, through the improvement of bradycardic response, despite not having reduced BP.

Resumo Fundamento: Os barorreceptores atuam como reguladores da pressão arterial (PA); no entanto, sua sensibilidade encontra-se prejudicada em pacientes hipertensos. Dentre as recomendações para a redução da PA, o treinamento físico tem se tornado um importante adjunto na terapia dessa população. Porém, ainda há diversos questionamentos sobre os efeitos de treinamento físico resistido nessa população. Objetivo: Avaliar o efeito do treinamento físico resistido na PA e na sensibilidade de barorreceptores em ratos espontaneamente hipertensos (SHR). Método: Ratos SHR (n = 16) e Wistar (n = 16) com 08 semanas de idade foram aleatoriamente divididos em 4 grupos: controle sedentário (CS, n = 8); controle treinado (CT, n = 8); SHR sedentário (HS, n = 8) e SHR treinado (HT, n = 8). O treinamento físico foi realizado em aparato com degraus (1,1 × 0,18 m, 2 cm entre os degraus, 80° inclinação) com peso fixado na cauda, (5 vezes por semana durante 8 semanas). O controle barorreflexo da frequência cardíaca (FC) foi testado com estímulos de fenilefrina e nitroprussiato de sódio. Resultados: O treinamento resistido foi capaz de aumentar a massa muscular do sóleo em ratos SHR (HS 0,027 ± 0,002 g/mm e HT 0,056 ± 0,003 g/mm). Não houve alteração da PA com o treinamento. Por outro lado, houve melhora na resposta bradicárdica da sensibilidade barorreflexa no grupo HT (HS -1,3 ± 0,1 bpm/mmHg e HT -2,6 ± 0,2 bpm/mmHg), no entanto, a resposta taquicárdica não foi alterada pelo exercício resistido (CS -3,3 ± 0,2 bpm/mmHg, CT -3,3 ± 0,1 bpm/mmHg, HS -1,47 ± 0,06 e HT -1,6 ± 0,1). Conclusão: O exercício físico resistido foi capaz de otimizar a sensibilidade barorreflexa dos ratos SHR por meio da melhora à resposta bradicárdica, apesar de não alterar a PA.

Evaluación de la Presencia de Disautonomía en Pacientes con Parkinson mediante el Análisis de Señales Cardiovasculares / Assessment of the Dysautonomia Presence in Parkinson disease through Cardiovascular Signal Analysis

Resumen: En este trabajo se evalúa y compara la respuesta del sistema nervioso autónomo (SNA) en pacientes con enfermedad de Parkinson (EP) y sujetos sanos para detectar la posible presencia de disautonomía. Las señales de electrocardiograma y fotopletismografía fueron adquiridas durante las maniobras: reposo, cambio de postura (Post-CP), respiración controlada (RC) e hiperventilación (Hip.). El análisis de las señales incluyó índices de la variabilidad de la frecuencia cardiaca (VFC) lineales y no lineales, índices de la señal de tiempo de tránsito de pulso y la sensibilidad del barorreflejo (índice α). Los pacientes con Parkinson mostraron una alteración en la modulación simpática principalmente durante Post-CP y una deficiencia en la respuesta cardiovagal en RC. La entropía aproximada disminuyó significativamente en sujetos sanos respecto a pacientes con EP durante RC. El índice α fue menor en pacientes con EP con respecto a sujetos sanos durante todo el protocolo, lo cual sugiere una alteración en el control del barorreflejo en EP. Sin embargo, es necesario aumentar el número de sujetos con la finalidad de determinar grados de disautonomía. El protocolo diseñado para evaluar la presencia de disautonomía en mexicanos con EP a través de señales no invasivas aportó información sobre el comportamiento del SNA.

Abstract: The goal of this work is to assess and to compare the autonomic nervous system (SNA) response in Parkinson's disease (EP) patients and healthy subjects in order to evaluate the possible dysautonomia presence. Electrocardiogram and photoplethysmography signals were acquired during the following maneuvers: rest, orthostatic change (Post-CP), controlled breathing (RC) and hyperventilation (Hip.). The signal processing was carried out by means of linear and no linear indices of heart rate variability (VFC), indices of pulse transit time (PTT) and baroreflex sensitivity (α index). Parkinson disease patients showed an attenuated sympathetic modulation mainly during Post-CP and the cardiovagal response resulted blunted during RC. Approximate entropy was significantly decreased in healthy subjects with respect to EP subjects during RC. In addition, the index α resulted in lower values in EP patients with respect to healthy subjects during the complete protocol, this result suggests that the baroreflex control in EP patients is blunted. However, is necessary to increase the number of subjects with the objective of determining levels of dysautonomia. The protocol designed to evaluate the dysautonomia presence in mexicans with EP through non invasive signals provides information about the SNA behavior.

Baroreflex deficit are associated with target organ damage / Os déficits de barorreflexo estão associados ao dano do órgão alvo

As is well known, there are different pathophysiological conditions in which baroreflex deficit is enrolled in end-organ damage like hypertension, heart failure and myocardial infarction. The purpose of this study was to investigate the mechanisms enrolled in those relationships using a baroreflex deficit­induced model. Sinoaortic-denervated (SAD) rats were used as a model of arterial baroreflex impairment. Male Wistar rats were divided into: control (n = 9), and SAD (n = 8, 30 days) groups. SAD was performed using the method previously described by Krieger (1964). Cardiac morphology was assessed by echocardiography BP, HR and BP, and pulse interval (PI) variabilities were analyzed using a data acquisition system (Codas, 2kHz). Stroke volume and peripheral and regional resistance were evaluated using colored microspheres. SAD induced LV hypertrophy estimated by LV/BW mass using echocardiography. BP (C: 106±0.6 vs. SAD: 108±2 mmHg) and HR (C: 355±7 vs. SAD: 357±15 bpm) were not modified by SAD, while BP variability (C: 6.2±0.84 vs SAD: 14±0.9 mmHg) and PI variability (C: 24±0.7 vs SAD:17±0.8 ms) were increased and decreased, respectively. Moreover, a reduction was observed in stroke volume (C: 0.31±0.02 vs SAD: 0.25±0.01 mL/ min) and an increase in total peripheral resistance (C: 0.97±0.07 vs. SAD: 1.23±0.07 mL/min/mmHg) in SAD animals. Those alterations resulted in increased cardiac vascular resistance (C: 35±1.6 vs. SAD:66±2.3 mmHg/mL/min/g) and renal vascular resistance (C: 31±1.2 vs. SAD: 75±2.2 mmHg/mL/min/g) in the SAD group. SAD induced an augment in cardiac and renal damage as cardiac morphology by histological techniques showed increased arterial wall and interstitial fibroses, and renal morphology showed interstitial fibroses and a decreased Bowmann space. Conclusion: Total baroreflex dysfunction impaired BP and HR variabilities associated with decreased stroke volume and increased peripheral and regional resistance. These adjustments may play an important role in target organ damage in different pathological conditions; even BP values were maintained at the control levels

Existem diferentes condições fisiopatológicas em que o déficit de barorreflexo está associado ao dano do órgão final, como hipertensão, insuficiência cardíaca e infarto do miocárdio. O objetivo deste estudo foi investigar os mecanismos inscritos nestes relacionamentos usando um modelo induzido por déficit de barorreflexo. Foram utilizados ratos com desnervação sino-aórtica (SAD) como modelo de comprometimento barorreflexo arterial. Os ratos Wistar machos foram divididos em grupos controle (n = 9) e SAD (n = 8, 30 dias). O SAD foi realizado utilizando o método anteriormente descrito por Krieger (1964). A morfologia cardíaca foi avaliada pela ecocardiografia PA, e as variabilidades de FC e PA, e do intervalo de pulso (IP) foram analisadas usando um sistema de aquisição de dados (Codas, 2kHz). O volume sistólico e a resistência periférica e regional foram avaliados utilizando microesferas coloridas. SAD induziu hipertrofia do VE estimada pela massa de VE/PC usando ecocardiografia. PA (C: 106±0,6 vs. SAD: 108±2 mmHg) e FC (C: 355±7 vs. SAD: 357±15 bpm) não foram modificados pelo SAD, enquanto a variabilidade da PA (C: 6,2±0,84 vs. SAD: 14±0,9 mmHg) e a variabilidade de PI (C: 24±0,7 vs. SAD: 17±0,8 ms) aumentaram e diminuíram, respectivamente. Além disso, observou-se uma redução no volume sistólico (C: 0,31± 0,02 vs SAD: 0,25 ± 0,01 mL/min) e um aumento na resistência periférica total (C: 0,97±0,07 vs. SAD: 1,23±0,07 mL/min/mmHg) em animais SAD. Essas alterações resultaram em aumento da resistência vascular cardíaca (C: 35±1,6 vs. SAD: 66 ± 2,3 mmHg/mL/min/g) e resistência vascular renal (C: 31±1,2 vs. SAD: 75±2,2 mmHg/mL/min/g) no grupo SAD. SAD induziu um aumento no dano cardíaco e renal como a morfologia cardíaca por técnicas histológicas mostrou aumento da parede arterial e fibrose intersticial, e a morfologia renal mostrou fibrose intersticial e uma diminuição do espaço de Bowmann. A disfunção barorreflexa total prejudicou as variabilidades de PA e FC associadas à diminuição do volume sistólico e ao aumento da resistência periférica e regional. Esses ajustes podem desempenhar um papel importante no dano de órgãos alvo em diferentes condições patológicas; até mesmo os valores da PA foram mantidos nos níveis de controle

New strategy for cardio-cerebrovascular diseases: baroreflex activation therapy / 药学实践杂志

The incident number and death toll of cardio-cerebrovascular diseases increase continuously in China.The impairment of arterial baroreflex (ABR) is closely related to the genesis and development of cardio-cerebrovascular diseases (such as hypertension and chronic heart failure).Barostim neoTM (by American CRVx.Inc) can reduce blood pressure and heart rate by electrically stimulating carotid sinus baroreceptors and activating baroreflex.Therefore, it can be used to treat resistant hypertension, heart failure and end-stage renal disease, etc.The mechanism of baroreflex activation therapy (BAT) includes inhibiting sympathetic nervous system and rennin-angiotensin system, and increasing the activity of vagus nerve.Thus it improves baroreflex sensitivity and heart rate variability, and restores the structure and function of key organs.

Mecanismos associados ao desenvolvimento das complicações cardiometabólicas em SHR submetidos à sobrecarga de frutose: papel do treinamento físico aeróbio / Mechanisms associated with cardiometabolic dysfunctions development in SHR submitted to fructose overload: role of aerobic exercise training

Neste estudo testamos a hipótese que alterações no controle autonômico precedem alterações cardiometabólicas em animais espontaneamente hipertensos tratados com frutose (SHR). Adicionalmente avaliamos os efeitos do treinamento físico aeróbio (TFA) no curso temporal das disfunções observadas neste modelo de síndrome metabólica. Para isso, foram utilizados ratos machos Wistar e SHR divididos em grupos (n=8): Controle (C), Hipertenso (H), Hipertenso+Frutose (HF) e Hipertenso+Frutose+Treinamento Físico (HFT). A sobrecarga de frutose (100g/L) e o TFA (esteira: 1h/d., 5d/sem.) foram iniciados 30 dias após o nascimento dos animais. Os grupos experimentais foram divididos em subgrupos que foram avaliados após 7, 15, 30 e 60 dias de protocolo. A partir dos 7 dias de protocolo a associação da hipertensão ao consumo de frutose (grupo HF) induziu redução da sensibilidade barorreflexa para respostas bradicárdicas (RB) e taquicárdicas (RT) em comparação ao grupo C; observando-se redução adicional da RB no grupo HF em relação ao grupo H (7 dias: -40% e 15 dias: -36%). A reatividade vascular à fenilefrina (8ug/ml: 7 aos 60 dias) estava prejudicada nos grupos H e HF em relação ao C; com prejuízo adicional do grupo HF ao nitroprussiato de sódio na dose de 20ug/ml (15 aos 60 dias de protocolo vs. C). Além disso, aos 15 e 30 dias de protocolo, o grupo HF apresentou um aumento marcante do TNFalfa e IL-6 no tecido adiposo e de IL-1beta no baço em relação aos grupos C e H. Houve redução de nitritos plasmáticos no grupo HF em 15 (55%) e 30 dias (58%) vs. o grupo C, acompanhado de aumento do peróxido de hidrogênio em 30 dias vs. o grupo H (98%). Em relação as defesas antioxidantes, o grupo HF apresentou menor atividade da superóxido dismutase (SOD) vs. os grupos C (15 dias: 36%, 30 dias: 31% e 60 dias: 47%) e H (15 dias: 25%, 30 dias: 21% e 60 dias: 43%), sem alterações significantes na catalase e no potencial antioxidante total. O grupo HF teve maior lipoperoxidação e oxidação de...

This study tested the hypothesis that changes in autonomic control precede cardiometabolic changes in spontaneously hypertensive rats (SHR) treated with fructose. Additionally, the effects of aerobic exercise training (AET) were evaluated in the time course of the dysfunctions observed in this metabolic syndrome model. Wistar and SHR rats were divided into groups (n=8/group): control (C), hypertensive (H), hypertensive + fructose (HF) and hypertensive + fructose + AET (HFT). The fructose overload (100g/l) and the AET (treadmill 1h/d, 5d/wk) was initiated at 30 days of life. The experimental groups were divided into subgroups, which were evaluated after 7, 15, 30 and 60 days of protocol. Since 7 day of protocol the association of hypertension and fructose consumption (HF group) induced a reduction in baroreflex sensitivity for bradycardic (BR) and tachycardia responses (TR) when compared to the C group; there was an additional reduction of BR in the HF group when compared to the H group (7 days: 40% and 15 days: 36%). The vascular reactivity to phenylephrine (8ug/ml: 7 to 60 days) was impaired in H and HF groups when compared to the C group; it was observed an additional impairment in the HF group to sodium nitroprusside at the dose of 20?g/ml (15 to 60 days of protocol vs. C). Additionally, at 15 and 30 day of protocol, the HF group showed an increase in TNFalfa and IL-6 in adipose tissue and in IL-1beta in the spleen when compared to C and H groups. There was a reduction in plasma nitrites in the HF group in 15 (55%) and 30 days of protocol (58%) vs. the C group, accompanied by an increase of the hydrogen peroxide in 30 days vs. H group (98%). Regarding the antioxidant defenses, the HF group showed reduced superoxide dismutase (SOD) activity as compared to C (15 days: 36%, 30 days: 31% and 60 days: 47%) and H groups (15 days: 25% 30 days: 21% and 60 days: 43%), without significant changes in catalase and in total antioxidant potential. The HF group had...