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AIMS: The carotid bodies are sensors that detect physiological signals and convey them to the central nervous system, where the stimuli are processed inducing reflexes through efferent pathways. Recent studies have demonstrated that electrical stimulation of the carotid sinus nerve (CSN) triggers the anti-inflammatory reflex under different conditions. However, whether this electrical stimulation attenuates colitis was never examined. This study aimed to evaluate if the electrical CSN stimulation attenuates the experimental colitis induced by intrarectal administration of acetic acid in rats. METHODS: Electrodes were implanted around the CSN to stimulate the CSN, and a catheter was inserted into the left femoral artery to record the arterial pressure. The observation of hypotensive responses confirmed the effectiveness of the electrical CNS stimulation. This maneuver was followed by a 4 % acetic acid or saline administered intrarectally. After 24 h, colons were segmented into distal and proximal parts for macroscopy, histological and biochemical assessment. KEY FINDINGS: As expected, the electrical CSN stimulation was effective in decreasing arterial pressure in saline and colitis rats. Moreover, electrical CSN stimulation effectively reduced colonic tissue lesions, colitis scores, and histopathologic parameters associated with colitis. In addition, the CSN stimulation also reduced the colonic mucosa pro-inflammatory cytokine interleukin-1 beta, and increased the anti-inflammatory interleukin-10, in rats submitted to colitis. SIGNIFICANCE: These findings indicated that electrical CSN stimulation breaks the vicious cycle of local colon inflammation in colitis, which might contribute to its better outcome.

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Different methods have been used to assess baroreflex gain in experiments where changes in the carotid sinus pressure or the arterial blood pressure using different techniques provoke a baroreflex response, usually a rapid variation of heart rate. Four mathematical models are most used in the literature: the linear regression, the piecewise regression, and two different four-parameter logistic equations: equation 1, Y = (A1-D1)/[1 + eB1(X - C1) ] + D1; equation 2, Y = (A2-D2)/[1 + (X/C2)B2 ] + D2. We compared the four models regarding the best fit to previously published data in all vertebrate classes. The linear regression had the worst fit in all cases. The piecewise regression generally exhibited a better fit than the linear regression, though it returned a similar fit when no breakpoints were found. The logistic equations showed the best fit among the tested models and were similar to each other. We demonstrate that equation 2 is asymmetric and the level of asymmetry is accentuated according to B2. This means that the baroreflex gain calculated when X = C2 is different from the actual maximum gain. Alternatively, the symmetric equation 1 returns the maximum gain when X = C1. Furthermore, the calculation of baroreflex gain using equation 2 disregards that baroreceptors may reset when individuals experience different mean arterial pressures. Finally, the asymmetry from equation 2 is a mathematical artifact inherently skewed to the left of C2, thus bearing no biological meaning. Therefore, we suggest that equation 1 should be used instead of equation 2.

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We present the case of a 75-year-old male with history of 5 months of right submaxillary tumor, with no clear etiology, who consulted for episodes of syncope preceded by dyspnea and sudden onset of profuse sweating. During his stay at the hospital, electrocardiographic records showed more than 3-second-long pauses after head movements, with a sensation of imminent loss of consciousness associated. A temporary pacemaker was required. Biopsy showed a diffuse non-germinal large B-cell B lymphoma, which required chemotherapy. After the first chemotherapy session, a significant reduction of the tumoral mass was observed, with abolition of the symptoms associated to cervical movements. The definitive diagnosis was malignant carotid sinus syndrome associated with cervical lymphoma.

Se describe el caso de un varón de 75 años con tumoración submaxilar derecha de 5 meses de evolución sin diagnóstico etiológico, que consultó por episodios de síncope precedidos por disnea y sudoración profusa de instalación súbita. Durante su internación se detectaron, en el monitoreo electrocardiográfico, pausas mayores a 3 segundos luego de la lateralización cervical reproduciendo los síntomas mencionados y asociadas a sensación de pérdida inminente de la conciencia, por lo que se implantó marcapasos transitorio. Se realizó biopsia de la masa tumoral cervical, consistente con linfoma B difuso de células grandes no centrogerminal, y se inició quimioterapia. Luego de dicho tratamiento quimioterápico se observó reducción significativa de la masa tumoral con abolición de los síntomas asociados a las maniobras cervicales. El diagnóstico definitivo fue síndrome del seno carotídeo maligno asociado a linfoma cervical.

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Baroreceptor and chemoreceptor reflexes modulate inflammatory responses. However, whether these reflexes attenuate periodontal diseases has been poorly examined. Thus, the present study determined the effects of electrical activation of the carotid sinus nerve (CSN) in rats with periodontitis. We hypothesized that activation of the baro and chemoreflexes attenuates alveolar bone loss and the associated inflammatory processes. Electrodes were implanted around the CSN, and bilateral ligation of the first mandibular molar was performed to, respectively, stimulate the CNS and induce periodontitis. The CSN was stimulated daily for 10 min, during nine days, in unanesthetized animals. On the eighth day, a catheter was inserted into the left femoral artery and, in the next day, the arterial pressure was recorded. Effectiveness of the CNS electrical stimulation was confirmed by hypotensive responses, which was followed by the collection of a blood sample, gingival tissue, and jaw. Long-term (9 days) electrical stimulation of the CSN attenuated bone loss and the histological damage around the first molar. In addition, the CSN stimulation also reduced the gingival and plasma pro-inflammatory cytokines induced by periodontitis. Thus, CSN stimulation has a protective effect on the development of periodontal disease mitigating alveolar bone loss and inflammatory processes.

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BACKGROUND: Cardioinhibitory carotid sinus hypersensitivity (CICSH) is defined as ventricular asystole ≥ 3 seconds in response to 5-10 seconds of carotid sinus massage (CSM). There is a common concern that a prolonged asystole episode could lead to death directly from bradycardia or as a consequence of serious trauma, brain injury or pause-dependent ventricular arrhythmias. OBJECTIVE: To describe total mortality, cardiovascular mortality and trauma-related mortality of a cohort of CICSH patients, and to compare those mortalities with those found in a non-CICSH patient cohort. METHODS: In 2006, 502 patients ≥ 50 years of age were submitted to CSM. Fifty-two patients (10,4%) were identified with CICSH. Survival of this cohort was compared with that of another cohort of 408 non-CICSH patients using Kaplan-Meier curves. Cox regression was used to examine the relation between CICSH and mortality. The level of statistical significance was set at 0.05. RESULTS: After a maximum follow-up of 11.6 years, 29 of the 52 CICSH patients (55.8%) were dead. Cardiovascular mortality, trauma-related mortality and the total mortality rate of this population were not statistically different from that found in 408 patients without CICSH. (Total mortality of CICSH patients 55.8% vs. 49,3% of non-CICSH patients; p: 0.38). CONCLUSION: At the end of follow-up, the 52 CICSH patient cohort had total mortality, cardiovascular mortality and trauma-related mortality similar to that found in 408 patients without CICSH.

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Abstract Background: Cardioinhibitory carotid sinus hypersensitivity (CICSH) is defined as ventricular asystole ≥ 3 seconds in response to 5-10 seconds of carotid sinus massage (CSM). There is a common concern that a prolonged asystole episode could lead to death directly from bradycardia or as a consequence of serious trauma, brain injury or pause-dependent ventricular arrhythmias. Objective: To describe total mortality, cardiovascular mortality and trauma-related mortality of a cohort of CICSH patients, and to compare those mortalities with those found in a non-CICSH patient cohort. Methods: In 2006, 502 patients ≥ 50 years of age were submitted to CSM. Fifty-two patients (10,4%) were identified with CICSH. Survival of this cohort was compared with that of another cohort of 408 non-CICSH patients using Kaplan-Meier curves. Cox regression was used to examine the relation between CICSH and mortality. The level of statistical significance was set at 0.05. Results: After a maximum follow-up of 11.6 years, 29 of the 52 CICSH patients (55.8%) were dead. Cardiovascular mortality, trauma-related mortality and the total mortality rate of this population were not statistically different from that found in 408 patients without CICSH. (Total mortality of CICSH patients 55.8% vs. 49,3% of non-CICSH patients; p: 0.38). Conclusion: At the end of follow-up, the 52 CICSH patient cohort had total mortality, cardiovascular mortality and trauma-related mortality similar to that found in 408 patients without CICSH.

Resumo Fundamento: A resposta cardioinibitória (RCI) à massagem do seio carotídeo (MSC) caracteriza-se por assistolia ≥ 3 segundos provocada por 5 a 10 segundos de MSC. Existe uma preocupação de que pacientes com RCI e episódios prolongados de assistolia possam falecer em consequência direta de bradiarritmia, ou em decorrência de lesão cerebral, trauma grave ou arritmia ventricular pausa dependente. Objetivos: Determinar a mortalidade total, a mortalidade cardiovascular e a mortalidade relacionada ao trauma de uma coorte de pacientes com RCI à MSC e comparar essas mortalidades com as de uma coorte de pacientes sem RCI à MSC. Métodos: Em 2006, 502 pacientes com idade igual ou superior a 50 anos foram submetidos à MSC. Destes, 52 pacientes (10,4%) foram identificados com RCI. A sobrevida desta coorte foi comparada àquela observada em uma coorte de 408 pacientes sem RCI por meio de curvas de Kaplan-Meier. A regressão de Cox foi utilizada para avaliação da relação entre a RCI à MSC e a mortalidade. Variáveis com p < 0,05 foram consideradas estatisticamente significativas. Resultados: Após seguimento máximo de 11,6 anos, 29 dos 52 portadores de RCI (55,8%) faleceram. A mortalidade total, a mortalidade cardiovascular e a mortalidade relacionada ao trauma desta coorte de pacientes não foram significativamente diferentes daquelas encontradas nos 408 pacientes sem RCI (mortalidade total com RCI: 55,8% versus 49,3% sem RCI; p: 0,38). Conclusões: No fim do seguimento, a mortalidade dos 52 portadores de RCI foi semelhante à observada em uma coorte de pacientes sem RCI. A mortalidade cardiovascular e a relacionada ao trauma também foi semelhante nas duas coortes.

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Electrical stimulation of the carotid baroreflex has been thoroughly investigated for treating drug-resistant hypertension in humans. However, a previous study from our laboratory, performed in conscious rats, has demonstrated that electrical stimulation of the carotid sinus/nerve (CS) activated both the carotid baroreflex as well as the carotid chemoreflex, resulting in hypotension. Additionally, we also demonstrated that the carotid chemoreceptor deactivation potentiated this hypotensive response. Therefore, to further investigate this carotid baroreflex/chemoreflex interaction, besides the hemodynamic responses, we evaluated the respiratory responses to the electrical stimulation of the CS in both intact (CONT) and carotid chemoreceptors deactivated (CHEMO-X) conscious rats. CONT rats showed increased ventilation in response to electrical stimulation of the CS as measured by the respiratory frequency (fR), tidal volume (VT) and minute ventilation (VE), suggesting a carotid chemoreflex activation. The carotid chemoreceptor deactivation abolished all respiratory responses to the electrical stimulation of the CS. Regarding the hemodynamic responses, the electrical stimulation of the CS caused hypotensive responses in CONT rats, which were potentiated by the carotid chemoreceptors deactivation. Heart rate (HR) responses did not differ between groups. In conclusion, the present study showed that the electrical stimulation of the CS, in conscious rats, activates both the carotid baroreflex and the carotid chemoreflex driving an increase in ventilation and a decrease in AP. These findings further contribute to our understanding of the electrical stimulation of CS.

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BACKGROUND: Carotid sinus hypersensitivity (CSH) is a frequent finding in the evaluation of syncope. However, its significance in the clinical setting is still dubious. A new criterion was proposed by Solari et al. with a symptomatic systolic blood pressure (SBP) cut-off value of ≤ 85 mmHg to refine the vasodepressor (VD) response diagnosis. OBJECTIVE: To determine and compare the response to carotid sinus massage (CSM) in patients with and without syncope according to standard and proposed criteria. METHODS: CSM was performed in 99 patients with and 66 patients without syncope. CSH was defined as cardioinhibitory (CI) for asystole ≥ 3 seconds, or as VD for SBP decrease ≥ 50 mmHg. RESULTS: No differences in the hemodynamic responses were observed during CSM between the groups, with 24.2% and 25.8% CI, and 8.1% and 13.6% VD in the symptomatic and asymptomatic groups, respectively (p = 0.466). A p value < 0.050 was considered statistically significant. During the maneuvers, 45 (45.45%) and 34 (51.5%) patients in the symptomatic and asymptomatic groups achieved SBP below ≤ 85 mmHg. Symptoms were reported especially in those patients in whom CSM caused a SBP decrease to below 90 mmHg and/or asystole > 2.5 seconds, regardless of the pattern of response or the presence of previous syncope. CONCLUSION: The response to CSM in patients with and without syncope was similar; therefore, CSH may be an unspecific condition. Clinical correlation and other methods of evaluation, such as long-lasting ECG monitoring, may be necessary to confirm CSH as the cause of syncope.

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Abstract Background: Carotid sinus hypersensitivity (CSH) is a frequent finding in the evaluation of syncope. However, its significance in the clinical setting is still dubious. A new criterion was proposed by Solari et al. with a symptomatic systolic blood pressure (SBP) cut-off value of ≤ 85 mmHg to refine the vasodepressor (VD) response diagnosis. Objective: To determine and compare the response to carotid sinus massage (CSM) in patients with and without syncope according to standard and proposed criteria. Methods: CSM was performed in 99 patients with and 66 patients without syncope. CSH was defined as cardioinhibitory (CI) for asystole ≥ 3 seconds, or as VD for SBP decrease ≥ 50 mmHg. Results: No differences in the hemodynamic responses were observed during CSM between the groups, with 24.2% and 25.8% CI, and 8.1% and 13.6% VD in the symptomatic and asymptomatic groups, respectively (p = 0.466). A p value < 0.050 was considered statistically significant. During the maneuvers, 45 (45.45%) and 34 (51.5%) patients in the symptomatic and asymptomatic groups achieved SBP below ≤ 85 mmHg. Symptoms were reported especially in those patients in whom CSM caused a SBP decrease to below 90 mmHg and/or asystole > 2.5 seconds, regardless of the pattern of response or the presence of previous syncope. Conclusion: The response to CSM in patients with and without syncope was similar; therefore, CSH may be an unspecific condition. Clinical correlation and other methods of evaluation, such as long-lasting ECG monitoring, may be necessary to confirm CSH as the cause of syncope.

Resumo Fundamento: A hipersensibilidade do seio carotídeo (HSC) é um achado frequente na avaliação da síncope. Entretanto, o valor da resposta positiva é ainda incerto no contexto clínico. Novo critério diagnóstico para tentar refinar a resposta vasodepressora (VD) foi proposto por Solari et al. com determinação da queda sintomática da pressão arterial sistólica (PAS) a níveis ≤ 85 mmHg como ponto de corte. Objetivo: Determinar e comparar a resposta à massagem do seio carotídeo (MSC) em pacientes com e sem síncope de acordo com os critérios vigentes e propostos. Métodos: A MSC foi realizada em 99 pacientes com síncope e 66 pacientes sem síncope. A HSC foi definida como cardioinibitória (CI), se assistolia ≥ 3 segundos, ou VD, se queda da PAS ≥ 50 mmHg. Resultados: Não foram observadas diferenças na resposta hemodinâmica entre os grupos durante a MSC, com 24,2% e 25,8% de resposta CI, e 8,1% e 13,6% de resposta VD nos grupos sintomático e assintomático, respectivamente (p = 0,466). Considerou-se p < 0,05 estatisticamente significativo. Durante as manobras, 45 (45,45%) e 34 (51,5%) pacientes nos grupos sintomático e assintomático atingiram PAS ≤ 85 mmHg. Sintomas foram relatados principalmente por pacientes em que a MSC reduziu a PAS para menos de 90 mmHg e/ou causou assistolia > 2,5 segundos, independentemente do padrão da resposta ou história de síncope prévia. Conclusão: As respostas à MSC em pacientes com e sem síncope foram semelhantes. Portanto, a HSC pode ser uma condição inespecífica. A correlação clínica mais precisa e outros métodos para avaliação, como monitoramento por ECG de longa duração, podem ser necessários para confirmação da HSC como causa da síncope.

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PURPOSE OF REVIEW: Surgical removal of the baroreceptor afferents [sino-aortic denervation (SAD)] leads to a lack of inhibitory feedback to sympathetic outflow, which in turn is expected to result in a large increase in mean arterial pressure (MAP). However, few days after surgery, the sympathetic nerve activity (SNA) and MAP of SAD rats return to a range similar to that observed in control rats. In this review, we present experimental evidence suggesting that breathing contributes to control of SNA and MAP following SAD.The purpose of this review was to discuss studies exploring SNA and MAP regulation in SAD rats, highlighting the possible role of breathing in the neural mechanisms of this modulation of SNA. RECENT FINDINGS: Recent studies show that baroreceptor afferent stimulation or removal (SAD) results in changes in the respiratory pattern. Changes in the neural respiratory network and in the respiratory pattern must be considered among mechanisms involved in the modulation of the MAP after SAD.

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Relata-se o caso de um paciente portador de marcapasso dupla-câ- mara, implantado por hipersensibilidade do seio carotídeo, que, em consulta ambulatorial, manifestou reaparecimento tardio dos sintomas que apresentava antes do implante do dispositivo. Após descartar alterações de limiares, sensibilidade ou impedância do sistema de estimulação cardíaca, foi realizada massagem do seio carotídeo e evidenciada inibição inadequada da estimulação ventricular. A radiografia de tórax revelou tratar-se de cabo-eletrodo ventricular posicionado em região látero-basal do ventrículo esquerdo via seio coronário. O problema foi corrigido com ajustes dos parâmetros, devidamente comprovado com a não reprodutibilidade do evento

We report the case of a patient with a dual-chamber pacemaker for carotid sinus hypersensitivity who, at an outpatient visit, presented a late resumption of the symptoms observed before the implantation of the device. After discarding threshold, sensitivity or impedance changes of the cardiac stimulation system, carotid sinus massage was performed and inadequate ventricular pacing inhibition was evidenced. A chest X-ray showed the ventricular lead had been placed at the laterobasal region of left ventricle through the coronary sinus. The problem was corrected by adjusting the parameters, and this was confirmed by a discontinuation of the event

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Recent studies demonstrated a critical functional connection between the autonomic (sympathetic and parasympathetic) nervous and the immune systems. The carotid sinus nerve (CSN) conveys electrical signals from the chemoreceptors of the carotid bifurcation to the central nervous system where the stimuli are processed to activate sympathetic and parasympathetic efferent signals. Here, we reported that chemoreflex activation via electrical CSN stimulation, in conscious rats, controls the innate immune response to lipopolysaccharide attenuating the plasma levels of inflammatory cytokines such as tumor necrosis factor (TNF), interleukin 1ß (IL-1ß) and interleukin 6 (IL-6). By contrast, the chemoreflex stimulation increases the plasma levels of anti-inflammatory cytokine interleukin 10 (IL-10). This chemoreflex anti-inflammatory network was abrogated by carotid chemoreceptor denervation and by pharmacological blockade of either sympathetic - propranolol - or parasympathetic - methylatropine - signals. The chemoreflex stimulation as well as the surgical and pharmacological procedures were confirmed by real-time recording of hemodynamic parameters [pulsatile arterial pressure (PAP) and heart rate (HR)]. These results reveal, in conscious animals, a novel mechanism of neuromodulation mediated by the carotid chemoreceptors and involving both the sympathetic and parasympathetic systems.

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Resumen:Este trabajo describe la presencia del cuerpo carotídeo y su relación con el seno carotídeo. Además, se presenta una revisión bibliográfica de la historia, anatomía y fisiologia del órgano y su importancia como quimioreceptor del cuerpo humano.

Abstract:This work describes the presence of carotid body and its relationship to the carotid sinus. In addition, a literature review of the history, anatomy and physiology of the body and its importance as chemoreceptory the human body is presented.

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BACKGROUND AND PURPOSE: Carotid bulb diaphragm (CBD) has been described in young carotid ischemic stroke (CIS) patients, especially in blacks. However, the prevalence of CBD in CIS patients is unknown, and whether CBD is a risk factor for CIS remains unclear. We assessed the association between CBD and incident CIS in a population-based study. METHODS: We selected all young (<55 years) CIS patients from a 1-year population-based cohort study in the Afro-Caribbean population of Martinique in 2012. All patients had a comprehensive work-up including a computed tomographic angiography. We calculated CIS associated with ipsilateral CBD incidence with 95% confidence intervals using Poisson distribution. We then selected age- and sex-matched controls among young (<55 years) Afro-Caribbean stroke-free patients admitted for a road crash who routinely had computed tomographic angiography. Odds ratio (ORs) were calculated by conditional logistic regression adjusted for hypertension, dyslipidemia, diabetes and smoking. RESULTS: CIS associated with ipsilateral CBD incidence was 3.8 per 100 000 person-years (95% confidence interval, 1.4-6.1). Prevalence of ipsilateral CBD was 23% in all CIS and 37% in undetermined CIS patients. When restricted to undetermined CIS, CBD prevalence was 24 times higher than that in controls (adjusted OR, 24.1; 95% confidence interval, 1.8-325.6). CONCLUSIONS: CBD is associated with an increased risk of ipsilateral CIS in young Afro-Caribbean population.

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Arterial baroreflex function is important for blood pressure control during exercise, but its contribution to cardiovascular adjustments at the onset of cycling exercise remains unclear. Fifteen healthy male subjects (24 ± 1 yr) performed 45-s trials of low- and moderate-intensity cycling, with carotid baroreceptor stimulation by neck suction at -60 Torr applied 0-5, 10-15, and 30-35 s after the onset of exercise. Cardiovascular responses to neck suction during cycling were compared with those obtained at rest. An attenuated reflex decrease in heart rate following neck suction was detected during moderate-intensity exercise, compared with the response at rest (P < 0.05). Furthermore, compared with the reflex decrease in blood pressure elicited at rest, neck suction elicited an augmented decrease in blood pressure at 0-5 and 10-15 s during low-intensity exercise and in all periods during moderate-intensity exercise (P < 0.05). The reflex depressor response at the onset of cycling was primarily mediated by an increase in the total vascular conductance. These findings evidence altered carotid baroreflex function during the first 35 s of cycling compared with rest, with attenuated bradycardic response, and augmented depressor response to carotid baroreceptor stimulation.

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Despite the abundance of evidence that supports the important role of aortic and carotid afferents to short-term regulation of blood pressure and detection of variation in the arterial PO2 , PCO2 and pH, relatively little is known regarding the role of these afferents during changes in the volume and composition of extracellular compartments. The present study sought to determine the involvement of these afferents in the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Sinoaortic-denervated and sham male Wistar rats were anaesthetised with intravenous (i.v.) urethane (1.2 g/kg body weight (bw)) prior to the measurement of the mean arterial pressure (MAP), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA). In the sham group, the HS infusion (3 mol/L NaCl, 1.8 mL/kg bw, i.v.) induced transient hypertension (12 ± 4 mmHg from baseline, peak at 10 min; P < 0.05), an increase in RVC (127 ± 9% and 150 ± 13% from baseline, at 20 and 60 min respectively; P < 0.05) and a decrease in RSNA (-34 ± 10% and -29 ± 5% from baseline, at 10 and 60 min respectively; P < 0.05). In sinoaortic-denervated rats, HS infusion promoted a sustained pressor response (30 ± 5 and 17 ± 6 mmHg of baseline values, at 10 and 30 min respectively; P < 0.05) and abolished the increase in RVC (85 ± 8% from baseline, at 10 min) and decrease in RSNA (-4 ± 3% from baseline, at 10 min). These results suggest that aortic and carotid afferents are involved in cardiovascular and renal sympathoinhibition responses induced by acute hypernatremia.

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