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Uncontrolled hypertension drives the global burden of increased cardiovascular disease (CVD) morbidity and mortality. Although high blood pressure (BP) is treatable and preventable, only half of the patients with hypertension undergoing treatment have their BP controlled. The failure of polypharmacy to attain adequate BP control may be due to a lack of physiological response, however, medication non-adherence and clinician inertia to increase treatment intensity are critical factors associated with poor hypertension management. The long-time medication titration, lifelong drug therapy, and often multi-drug treatment strategy are frustrating when the BP goal is not achieved, leading to increased CVD risk and a substantial burden on the healthcare system. Growing evidence indicates that neurohumoral activation is critical in initiating and maintaining elevated BP and its adverse consequences. Over the past decades, device-based therapies targeting the mechanisms underlying hypertension pathophysiology have been extensively studied. Among these, robust clinical experience for hypertension management exists for renal denervation (RDN) and baroreflex activation therapy (BAT), carotid body denervation (CBD), central arteriovenous anastomosis, and to a lesser extent, deep brain stimulation. Future studies are warranted to define the role of device-based approaches as an alternative or adjunctive treatment option to treat hypertension. Systemic hypertension is a growing contributor to global disease burden and premature cause of death worldwide. The percentage of patients achieving target BP levels remains largely inadequate. Hypertension is characterised by activation of the sympathetic nervous system, with the magnitude depending on age and the disease severity. Device-based interventions have been extensively studied to directly target the relevant sympathetic neural pathophysiological mechanisms involved in BP control. Modulation of the chronic sympathetic outflow with CBD or BAT shows promise for the treatment of poorly controlled hypertension in addition to antihypertensive medicines. The BP response to device-based therapies appears variable and cannot be predicted before the procedure. Until more robust evidence related to patient selection, procedural and technical aspects is available, chemoreflex and baroreflex neuromodulation therapy should be restricted to randomised sham-controlled trials performed in experienced centres. [ABSTRACT FROM AUTHOR]

Background: Carotidwebs are nonatherosclerotic fibrous bands thatmay alter hemodynamic flowand increase the risk of platelet aggregation, leading to thromboembolism in young, otherwise healthy individuals. Although rare, carotid webs are important causes of thromboembolic strokes and are of ten overlooked in the routineworkup for a stroke. Treating physicians and radiologists must recognize and properly manage patients who present with carotid webs to prevent recurrent thromboembolism. Case Report: A healthy 30-year-old female presented with slurred speech and unilateral left upper and lower extremity numbness. Imaging modalities showed an acute infarction of the right middle cerebral artery and bilateral carotid webs. The patient was managed operatively with a right carotid endarterectomy and discharged on day 3 of admission on a regimen of ticagrelor, amlodipine, and aspirin. The patient was asymptomatic at 1-year follow-up. Conclusion: Our case highlights the clinical relevance of considering carotid web as a potential etiology for ischemic stroke in young, otherwise healthy patients and emphasizes the importance of timely diagnosis and appropriate management to prevent recurrent cerebrovascular events. [ABSTRACT FROM AUTHOR]

Uncontrolled hypertension drives the global burden of increased cardiovascular disease (CVD) morbidity and mortality. Although high blood pressure (BP) is treatable and preventable, only half of the patients with hypertension undergoing treatment have their BP controlled. The failure of polypharmacy to attain adequate BP control may be due to a lack of physiological response, however, medication non-adherence and clinician inertia to increase treatment intensity are critical factors associated with poor hypertension management. The long-time medication titration, lifelong drug therapy, and often multi-drug treatment strategy are frustrating when the BP goal is not achieved, leading to increased CVD risk and a substantial burden on the healthcare system. Growing evidence indicates that neurohumoral activation is critical in initiating and maintaining elevated BP and its adverse consequences. Over the past decades, device-based therapies targeting the mechanisms underlying hypertension pathophysiology have been extensively studied. Among these, robust clinical experience for hypertension management exists for renal denervation (RDN) and baroreflex activation therapy (BAT), carotid body denervation (CBD), central arteriovenous anastomosis, and to a lesser extent, deep brain stimulation. Future studies are warranted to define the role of device-based approaches as an alternative or adjunctive treatment option to treat hypertension.

IntroductionEarly promising results of renal nerve denervation awakened interest in developing medical device alternatives for patients with resistant hypertension. The subsequent sham-controlled renal nerve denervation randomized trials were disappointing leading researchers and innovators to explore alternative device and trial designs to address this significant unmet need. We describe the innovation process leading to the first endovascular carotid baroreflex amplification device currently undergoing clinical trials in the United States and Europe.Areas coveredWe provide a brief overview of carotid baroreceptor physiology and then couple this knowledge with the fundamental principles of strain pattern changes that led to the proposed innovation. The mechanism of blood pressure reduction via enhancing innate physiologic carotid sinus baroreceptor signaling through changes in pulsatile focal carotid bulb strain is described alongside preclinical testing and early clinical results.Expert opinionThe collective data to date suggest endovascular carotid baroreflex amplification may be an innovative alternative for resistant hypertension patients. However, well-controlled studies will be needed to assess efficacy, safety, durability, and risk: benefit of this permanent intravascular carotid implant.Subject codeshigh blood pressure, hypertension, treatment, physiology.

Violence against the neck can result in a range of macromorphological and micromorphological findings. However, the forensic relevance of the carotid sinus in cases of violence against the neck remains controversial. In this follow-up study of 22 cases of suicidal and accidental strangulations, carotid bifurcations were examined histologically for morphological changes implying direct trauma, including haemorrhage and immunohistochemical expression of heat-shock proteins 27, 60, and 70 and aquaporin-3. These cases were compared with a control group (82 cases) without neck compression or head trauma and with variable causes of death. No relevant histopathological findings implying direct trauma of the carotid bifurcation were found. No cases showed positive aquaporin-3 staining and only five cases showed positive heat-shock protein-27 staining, all of which were hangings. Without massive trauma of the carotid bifurcation, histological alterations cannot be expected. Without signs of rapid death, findings of acute circulatory failure, macromorphological and micromorphological findings of neck compression, and reliable markers indicating relevant impact on the carotid bifurcation the diagnosis of a lethal reflex cannot be verified.Key pointsAmong 22 cases of strangulation causing death, there were 16 cases of hanging and 6 cases of ligature strangulationFew cases showed small haemorrhages located predominantly in the surrounding fat and connective tissues; however, the haemorrhages did not have any effects on the tissuesNeck compression had minimal effects on heat shock protein 27 expression in carotid artery tissueAquaporin-3 staining suggested it is not a useful marker for relevant neck pressure, or that there had not been any relevant neck impactOur findings suggested no direct evidence for reflex cardiac death resulting from a brief force against the neck

Rationale: Syncope is a common condition in emergency departments, posing a diagnostic challenge due to its multifactorial nature. Among the potential causes, carotid sinus hypersensitivity leading to carotid sinus syndrome (CSS) is a significant consideration that can severely impact patient quality of life. Despite its importance, establishing effective treatment methods for CSS has been difficult., Patient Concerns: A 43-year-old male presented with recurrent episodes of syncope, which significantly affected his daily life and well-being., Diagnoses: After a thorough evaluation, the patient was diagnosed with CSS, a condition that can be difficult to pinpoint and requires specialized diagnostic procedures to confirm., Interventions: The patient was treated with stellate ganglion block therapy, a targeted intervention aimed at addressing the underlying cause of CSS. This treatment was administered over a 12-day period., Outcomes: Following the treatment, the patient's symptoms showed gradual improvement, and he was discharged after meeting the clinical cure criteria. During a 7-month follow-up, he remained symptom-free., Lessons: The case highlights the effectiveness of transcutaneous stellate ganglion block therapy in treating CSS. It suggests that further research and clinical trials are needed to validate this treatment's efficacy, potentially offering a new therapeutic option for patients suffering from CSS., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Violence against the neck can result in a range of macromorphological and micromorphological findings. However, the forensic relevance of the carotid sinus in cases of violence against the neck remains controversial. In this follow-up study of 22 cases of suicidal and accidental strangulations, carotid bifurcations were examined histologically for morphological changes implying direct trauma, including haemorrhage and immunohistochemical expression of heat-shock proteins 27, 60, and 70 and aquaporin-3. These cases were compared with a control group (82 cases) without neck compression or head trauma and with variable causes of death. No relevant histopathological findings implying direct trauma of the carotid bifurcation were found. No cases showed positive aquaporin-3 staining and only five cases showed positive heat-shock protein-27 staining, all of which were hangings. Without massive trauma of the carotid bifurcation, histological alterations cannot be expected. Without signs of rapid death, findings of acute circulatory failure, macromorphological and micromorphological findings of neck compression, and reliable markers indicating relevant impact on the carotid bifurcation the diagnosis of a lethal reflex cannot be verified. Among 22 cases of strangulation causing death, there were 16 cases of hanging and 6 cases of ligature strangulation Few cases showed small haemorrhages located predominantly in the surrounding fat and connective tissues; however, the haemorrhages did not have any effects on the tissues Neck compression had minimal effects on heat shock protein 27 expression in carotid artery tissue Aquaporin-3 staining suggested it is not a useful marker for relevant neck pressure, or that there had not been any relevant neck impact Our findings suggested no direct evidence for reflex cardiac death resulting from a brief force against the neck [ABSTRACT FROM AUTHOR]

Death after carotid sinus trauma is usually attributed to death from inhibition, a type of sudden death. Currently, the number of incidents is scarce, and related studies are few. Therefore, how to determine the involvement of carotid sinus and determine the role of diseases in the cause of death has always been a difficult point in forensic investigation. This article sorts out the research literature on carotid sinus related death at home and abroad in recent years, systematically reviews the anatomic structure of the carotid sinus nerve, the clinical epidemiology of carotid sinus syndrome, and the research on the death mechanism of carotid sinus injury at home and abroad in recent years, in order to provide references for forensic pathology research and prosecution.

Abstract Background The risk of stroke after carotid sinus massage is greater if there is preexisting carotid stenosis or carotid plaques. We present the case of a patient with underlying 40% carotid stenosis, who developed a watershed stroke after a self-neck massage in our stroke unit. We show a well-documented case with magnetic resonance images before and after the neck massage. We report a case of a watershed brain infarct after a self-massage of the carotid sinus, with preexisting carotid artery stenosis. Neck massage continues to be a significant cause of stroke and should therefore not be performed by patients. Clinicians must be aware of the implications of a carotid sinus massage in both the outpatient and inpatient settings. Case presentation We admitted a 58-year-old white male patient, with no relevant medical history, to our department with a brain stem infarct. During his stay at our stroke unit, the patient performed a self-neck massage with consecutive bradycardia and asystole, resulting in left-side hemiparesis. The underlying cause of the hemodynamic stroke is believed to be secondary to this intensive neck massage performed by the patient. The patient also suffered from unknown right internal carotid artery stenosis. Conclusion Clinicians and patients must be aware that neck massage can lead to ischemic stroke. We postulate that repetitive impaired cardiac output can lead to a hemodynamic (watershed-type) stroke.

Introduction: Carotid sinus syndrome (CSS) is a hypersensitivity of the carotid sinus manifested by atrioventricular sinus bradycardia or decreased arterial pressure of at least 50 mmHg. Triggering factors can be neck movements, shaving of the beard or too-tight collars. CSS can be rarely caused by the presence of malignant or benign masses in the head and neck area. Case Report: A 49 years-old white woman with a laterocervical mass presented recurrent episodes of sinus bradycardia related to head’s rotation. Neck CT scan revealed a right piolaryngocele and internal left laryngocele. Episodes of bradycardia were disappeared after endolaryngeal carbon dioxide laser assisted marsupialization. Conclusion: Laryngocele should be sought in the differential diagnosis of patients with bradycardia episodes due to carotid sinus compression. Surgical treatment of laryngoceles can lead to the termination of such episodes.

Histomorphological study confirmed that the carotid sinus was characterized by an abrupt thinning of elastic tunica media which was rapidly replaced by the normal muscularity of the media on the distal progression in the internal carotid artery. The carotid sinus was richly supplied with sensory receptors which took the form of menisci and left the sinus as the nerve of Hering.

Surgery on head and neck masses presents unique challenges to overcome, especially in relation to preoperative anesthesia induction. Tumor proximity to the carotid sinus can result in extreme hemodynamic depression, by way of compression or direct invasion of the node. Neck hyperextension required for endotracheal intubation can worsen the underlying compression. Additionally, many anesthetic agents have sympatholytic properties that can exacerbate this imbalance further toward the parasympathetic response. We present a case of a patient with non-Hodgkin lymphoma whose tumor compression of the carotid sinus precipitated an exaggerated vagal reflex response following fentanyl administration., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Vrionis et al.)

Animals have evolved homeostatic responses to changes in oxygen availability that act on different timescales. Although the hypoxia-inducible factor (HIF) transcriptional pathway that controls long-term responses to low oxygen (hypoxia) has been established, the pathway that mediates acute responses to hypoxia in mammals is not well understood. Here we show that the olfactory receptor gene Olfr78 is highly and selectively expressed in oxygen-sensitive glomus cells of the carotid body, a chemosensory organ at the carotid artery bifurcation that monitors blood oxygen and stimulates breathing within seconds when oxygen declines. Olfr78 mutants fail to increase ventilation in hypoxia but respond normally to hypercapnia. Glomus cells are present in normal numbers and appear structurally intact, but hypoxia-induced carotid body activity is diminished. Lactate, a metabolite that rapidly accumulates in hypoxia and induces hyperventilation, activates Olfr78 in heterologous expression experiments, induces calcium transients in glomus cells, and stimulates carotid sinus nerve activity through Olfr78. We propose that, in addition to its role in olfaction, Olfr78 acts as a hypoxia sensor in the breathing circuit by sensing lactate produced when oxygen levels decline.

The association between blood viscosity and pathological conditions involving a number of organ systems is well known. However, how the body measures and maintains appropriate blood viscosity is not well-described. The literature endorsing the function of the carotid sinus as a site of baroreception can be traced back to some of the earliest descriptions of digital pressure on the neck producing a drop in blood delivery to the brain. For the last 30 years, improved computational fluid dynamic (CFD) simulations of blood flow within the carotid sinus have demonstrated a more nuanced understanding of the changes in the region as it relates to changes in conventional metrics of cardiovascular function, including blood pressure. We suggest that the unique flow patterns within the carotid sinus may make it an ideal site to transduce flow data that can, in turn, enable real-time measurement of blood viscosity. The recent characterization of the PIEZO receptor family in the sinus vessel wall may provide a biological basis for this characterization. When coupled with other biomarkers of cardiovascular performance and descriptions of the blood rheology unique to the sinus region, this represents a novel venue for bioinspired design that may enable end-users to manipulate and optimize blood flow.

Background: The risk of stroke after carotid sinus massage is greater if there is preexisting carotid stenosis or carotid plaques. We present the case of a patient with underlying 40% carotid stenosis, who developed a watershed stroke after a self-neck massage in our stroke unit. We show a well-documented case with magnetic resonance images before and after the neck massage. We report a case of a watershed brain infarct after a self-massage of the carotid sinus, with preexisting carotid artery stenosis. Neck massage continues to be a significant cause of stroke and should therefore not be performed by patients. Clinicians must be aware of the implications of a carotid sinus massage in both the outpatient and inpatient settings.Case Presentation: We admitted a 58-year-old white male patient, with no relevant medical history, to our department with a brain stem infarct. During his stay at our stroke unit, the patient performed a self-neck massage with consecutive bradycardia and asystole, resulting in left-side hemiparesis. The underlying cause of the hemodynamic stroke is believed to be secondary to this intensive neck massage performed by the patient. The patient also suffered from unknown right internal carotid artery stenosis.Conclusion: Clinicians and patients must be aware that neck massage can lead to ischemic stroke. We postulate that repetitive impaired cardiac output can lead to a hemodynamic (watershed-type) stroke. [ABSTRACT FROM AUTHOR]

Introduction: Carotid sinus syndrome (CSS) is a hypersensitivity of the carotid sinus manifested by atrioventricular sinus bradycardia or decreased arterial pressure of at least 50 mmHg. Triggering factors can be neck movements, shaving of the beard or too-tight collars. CSS can be rarely caused by the presence of malignant or benign masses in the head and neck area. Case Report: A 49 years-old white woman with a laterocervical mass presented recurrent episodes of sinus bradycardia related to head's rotation. Neck CT scan revealed a right piolaryngocele and internal left laryngocele. Episodes of bradycardia were disappeared after endolaryngeal carbon dioxide laser assisted marsupialization. Conclusion: Laryngocele should be sought in the differential diagnosis of patients with bradycardia episodes due to carotid sinus compression. Surgical treatment of laryngoceles can lead to the termination of such episodes. [ABSTRACT FROM AUTHOR]

Abstract Objective This study aims to use a wall shear stress (WSS) quantitative analysis software to analyze and evaluate the carotid sinus WSS spatial distribution and characteristics in intima-media thickness (IMT) normal and thickening group by using two-dimensional color doppler flow imaging (CDFI) so as to assist clinicians to predict the location and risk of plaque formation. Methods According to IMT, 50 subjects was selected as IMT thickening group and 50 subjects as IMT normal group from subjects who had a carotid ultrasound examination in Shanghai East hospital during October 2016 to October 2017. This study presents the spatial distribution of the carotid sinus WSS based on the WSS quantitative analysis software and compared the spatial distribution and characteristics of the carotid sinus WSS between IMT thickening group and IMT normal group through two- and three-dimensional WSS maps and a fused WSS image. Results The distributional regularity of WSS in both two group was: carotid sinus

Nighttime blood pressure (BP) generally dips by 10% to 20% of the daytime values, and abnormal BP dipping may affect vascular health independently of BP level. The regulation of BP dipping involves arterial baroreflex, whose receptors mainly reside in carotid sinuses and aortic arch. Atherosclerosis in these baroreceptor-resident arteries (BRAs) is frequent among patients with ischemic stroke (IS) and might impair their BP-regulating capacity. We aimed to examine associations between atherosclerosis of BRA and BP dipping in patients with IS. BP dipping ratio was measured by 24-hour ambulatory blood pressure monitoring on the sixth day after IS. With computed tomography angiography, atherosclerosis conditions in 10 segments of carotid sinuses and aortic arch were scored and summed as total atherosclerosis burden of BRA. Among the 245 patients with IS, 78.0% had atherosclerosis in BRA. The total AS burden of BRA was negatively correlated with systolic BP dipping ratio (r=-0.331; P<0.001) and diastolic BP dipping ratio (r=-0.225; P<0.001). After adjusting for age, sex, vascular risk factors, 24-hour BP means, cervical and intracranial atherosclerosis scores, the negative correlations still existed (adjusted β, -0.259 [95% CI, -0.416 to -0.102] and adjusted β, -0.178 [95% CI, -0.346 to -0.010], respectively). In conclusion, higher total atherosclerosis burden of BRA was independently indicative of more blunted dipping of systolic BP and diastolic BP in IS. The total atherosclerosis burden of BRA might be important for predicting and managing BP dipping in patients with IS. [ABSTRACT FROM AUTHOR]

Arterial baroreflex activation through electrical carotid sinus stimulation has been developed for the treatment of resistant hypertension. Previous studies suggested that the peripheral chemoreflex is tonically active in hypertensive patients and may inhibit baroreflex responses. We hypothesized that peripheral chemoreflex activation attenuates baroreflex efficacy evoked by electrical carotid sinus stimulation. We screened 35 patients with an implanted electrical carotid sinus stimulator. Of those, 11 patients with consistent acute depressor response were selected (7 men/4 women, age: 67±8 years, body mass index: 31.6±5.2 kg/m2, 6±2 antihypertensive drug classes). We assessed responses to electrical baroreflex stimulation during normoxia, isocapnic hypoxia (SpO2: 79.0±1.5%), and hyperoxia (40% end-tidal O2 fraction) by measuring heart rate, blood pressure, ventilation, oxygen saturation, end-tidal CO2 and O2 fractions, and muscle sympathetic nerve activity. During normoxia, baroreflex activation reduced systolic blood pressure from 164±27 to 151±25 mm Hg (mean±SD, P<0.001), heart rate from 64±13 to 61±13 bpm (P=0.002), and muscle sympathetic nerve activity from 42±12 to 36±12 bursts/min (P=0.004). Hypoxia increased systolic blood pressure 8±12 mm Hg (P=0.057), heart rate 10±6 bpm (P<0.001), muscle sympathetic nerve activity 7±7 bursts/min (P=0.031), and ventilation 10±7 L/min (P=0.002). However, responses to electrical carotid sinus stimulation did not differ between hypoxic and hyperoxic conditions: systolic blood pressure: -15±7 versus -14±8 mm Hg (P=0.938), heart rate: -2±3 versus -2±2 bpm (P=0.701), and muscle sympathetic nerve activity: -6±4 versus -4±3 bursts/min (P=0.531). We conclude that moderate peripheral chemoreflex activation does not attenuate acute responses to electrical baroreflex activation therapy in patients with resistant hypertension. These patients provided insight into human baroreflex-chemoreflex interactions that could not be gained otherwise. [ABSTRACT FROM AUTHOR]

Afferent baroreflex failure is most often due to damage of the carotid sinus nerve because of neck surgery or radiation. The clinical picture is characterized by extreme blood pressure lability with severe hypertensive crises, hypotensive episodes, and orthostatic hypotension, making it the most difficult form of hypertension to manage. There is little evidence-based data to guide treatment. Recommendations rely on understanding the underlying pathophysiology, relevant clinical pharmacology, and anecdotal experience. The goal of treatment should be improving quality of life rather than normalization of blood pressure, which is rarely achievable. Long-acting central sympatholytic drugs are the mainstay of treatment, used at the lowest doses that prevent the largest hypertensive surges. Short-acting clonidine should be avoided because of rebound hypertension, but can be added to control residual hypertensive episodes, often triggered by mental stress or exertion. Hypotensive episodes can be managed with countermeasures and short-acting pressor agents if necessary. [ABSTRACT FROM AUTHOR]

A morphological study of 200 atherosclerotic carotid sinus (CS)plaques obtained at carotid endarterectomy revealed the structuralcomponents and processes characteristic for severe atherosclerosis:foci of atheromatosis and edema, necrosis of collagenand elastic fibres, newly formed vessels and hemorrhages of variousduration, lipophages and lymphocytes, portions of fibrosisand calcification, covering thinning and ulceration, thrombi andthe contents of plaques (atheromatous masses, cholesterol crystals,lipophages, calcificates) on their surface. Clinical and morphologicalcomparisons indicated that patients with ischemicstroke in their history had more severe atherosclerosis than thosewith asymptomatic CS stenosis. They were more commonlyfound to have vulnerable atherosclerotic plaques that showed apredominance of atheromatosis foci over the portions of fibrosisand calcification, covering thinning and destruction, formationof thrombi on its surface. It was ascertained that concomitantarterial hypertension might play a crucial role in the pathogenesisof hemorrhages into the atherosclerotic CS plaque.

The hemodynamic milieu differs throughout the vascular tree because of varying vascular geometry and blood velocities. Accordingly, the risk of turbulence, which is dictated by the Reynolds and Dean numbers, also varies. Relatively high blood viscosity is needed to prevent turbulence in the left ventricle and aorta, where high-velocity blood changes direction several times. Low blood viscosity is needed in the capillaries, where erythrocytes pass through vessels with a diameter smaller than their own. In addition, higher blood viscosity is necessary when the cardiac output and peak blood velocity increase as a part of a sympathetic response or anemia, which occurs following significant hemorrhage. Blood viscosity, as reflected in systemic vascular resistance and vascular wall shear stress, is sensed, respectively, by cardiomyocyte stretching in the left ventricle and mechanoreceptors for wall shear stress in the carotid sinus. By controlling blood volume and red blood cell mass, the renin-aldosterone-angiotensin system and the systemic vascular resistance response control the hematocrit, the strongest intrinsic determinant of blood viscosity. These responses provide gross control of blood viscosity. Fine-tuning of blood viscosity in transient conditions is provided by hormonal control of erythrocyte deformability. The short half-life of some of these hormones limits their activity to specific vascular beds. Hormones that modulate blood viscosity include erythropoietin, angiotensin II, brain natriuretic factor, epinephrine, prostacyclin E2, antidiuretic hormone, and nitric oxide., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Sloop et al.)

Cerebral autoregulation is an important factor in prevention of cerebral ischemic events. We tested a traditional but unproven hypothesis that carotid sinus baroafferent signals contribute to dynamic cerebral autoregulation. Middle cerebral artery mean blood velocity (MCA V mean ) responses to thigh-cuff deflation-induced acute hypotension were compared between conditions using neck suction soon after cuff deflation, without or with a cushion wrapped around the upper neck, in nine healthy males (aged 25 ± 5 years). Neck suction was applied close to the hypotension. The MCA V mean response was expected to differ between conditions because the cushion was presumed to prevent the carotid sinus distension by neck suction. The cushion hindered bradycardia and depressor responses during sole neck suction. Thigh-cuff deflation decreased mean arterial blood pressure (MAP) and MCA V mean (Ps < 0.05) with an almost unchanged respiratory rate under both conditions. However, in the neck suction + cushion condition, subsequent MCA V mean restoration was faster and greater (Ps ≤ 0.0131), despite similar changes in MAP in both conditions. Thus, carotid sinus baroafferent signals would accelerate dynamic cerebral autoregulation during rapid hypotension in healthy young males. Elucidating the mechanism underlying cerebral neural autoregulation could provide a new target for preventing cerebral ischemic events., (© 2024 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Background: Patients undergoing carotid endarterectomy (CEA) have a high restenosis rate, which increases the risk of stroke, and there is still a lack of effective treatment for restenosis. The cause of stenosis is related to local inflammatory reactions. Some basic studies have shown that the inflammatory response causing arterial stenosis is closely related to the nerve axons distributed in its outer membrane, and that removal of the nerve is effective in reducing the inflammatory response to prevent arterial stenosis. Therefore, we propose to design a randomized controlled trial to study whether disconnecting the carotid sinus nerve during a CEA operation can reduce carotid arterial restenosis., Method/design: This study is a randomized, double-blind, single-center study. We will recruit 276 patients, who will be randomly divided into the experimental group and the control group. Based on the standard CEA operation, the operator will search for the carotid sinus nerve on the surface of the internal carotid artery and will entirely transect it in the experimental group. Both groups will be guided with the same postoperative treatment and will be followed up every 3 months for 3 years after the operation. The main indices observed will be the carotid restenosis rate, incidence and nature of carotid plaque, and carotid blood flow velocity. Other indices will be arrhythmia, blood pressure variability, and biomarkers of atherosclerosis, such as blood lipids, hypersensitive C-reactive protein (hs-CRP), homocysteine, and total bilirubin., Discussion: It is expected that carotid sinus nerve transection will significantly reduce the occurrence of restenosis after CEA, decrease the incidence of ischemic stroke, and realize the effective primary prevention of stroke., Trial Registration: ChiCTR2300073652. Registered on July 18, 2023., (© 2024. The Author(s).)

New Findings: What is the central question of this study?Does carotid body input contribute to the hyperosmotic responses?What is the main finding and its importance?The response to NaCl overload is sympathorespiratory excitation. Eliminating the carotid body input reduced sympathoexcitation but did not affect the increase in phrenic burst frequency, whereas eliminating the hypothalamus prevented the tachypnoea and sympathoexcitation. We conclude that the carotid body inputs are essential for the full expression of the sympathetic activity during acute NaCl overload, whereas the tachypnoea depends on hypothalamic mechanisms. Acute salt excess activates central osmoreceptors, which trigger an increase in sympathetic and respiratory activity. The carotid bodies also respond to hyperosmolality of the extracellular compartment, but their contribution to the sympathoexcitatory and ventilatory responses to NaCl overload remains unknown. To evaluate their contribution to acute NaCl overload, we recorded thoracic sympathetic (tSNA), phrenic (PNA) and carotid sinus nerve activities in decorticate in situ preparations of male Holtzman rats (60–100 g) while delivering intra‐arterial infusions of hyperosmotic NaCl (0.17, 0.3, 0.7, 1.5 and 2.0 mol l−1; 200 μl infusion over 25–30 s, with a 10 min time interval between solutions) or mannitol (0.3, 0.5, 1.0, 2.7 and 3.8 mol l−1) progressively. The cumulative infusions of hyperosmotic NaCl increased the perfusate osmolality to 341 ± 5 mosmol (kg water)−1 and elicited an immediate increase in PNA and tSNA (n = 6, P < 0.05) in sham‐denervated rats. Carotid body removal attenuated sympathoexcitation (n = 5, P < 0.05) but did not affect the tachypnoeic response. A precollicular transection disconnecting the hypothalamus abolished the sympathoexcitatory and tachypnoeic responses to NaCl overload (n = 6, P < 0.05). Equi‐osmolar infusions of mannitol did not alter the PNA and tSNA in sham‐denervated rats (n = 5). Sodium chloride infusions increased carotid sinus nerve activity (n = 10, P < 0.05), whereas mannitol produced negligible changes (n = 5). The results indicate that carotid bodies are activated by acute NaCl overload, but not by mannitol. We conclude that the carotid bodies contribute to the increased sympathetic activity during acute NaCl overload, whereas the ventilatory response is mainly mediated by hypothalamic mechanisms. [ABSTRACT FROM AUTHOR]

Carotid rete mirabile is an arterial meshwork, occurring at the cavernous portion of the internal carotid artery (ICA). Rete mirabile in humans is not present during normal development of the intracranial circulation and hence is considered as a collateral pathway that develops as a consequence of segmental agenesis of the ICA. We report three cases of this rare entity encountered at our institute. [ABSTRACT FROM AUTHOR]

Background: The carotid sinus (CS) is a dilatation in the carotid bifurcation usually at the origin of proximal internal carotid artery (ICA). It contains baroreceptors which influence blood pressure. Variations in the location of the CS are of importance as atheromatous plaque commonly forms in this area and procedures such as carotid endarterectomy are performed to reduce the risk of stroke. Inadvertent stimulation of the CS baroreceptors during interventions can have profound effects on the patient's haemodynamic status both intra- and postoperatively, causing serious complications. The aim of this study is to determine the inter- and intra-individual variations in the location of the CS.Materials and Methods: Eighty-two carotid arteries were dissected bilaterally from 41 cadavers. The locations of the CS were noted and divided into four potential sites.Results: The commonest site is the origin of the ICA (74.3%), but the CS can also be found in the distal part of the common carotid artery (CCA) inferior to the bifurcation (17.1%); at the bifurcation involving the distal CCA and origins of both the external carotid artery (ECA) and ICA (7.32%); and at the origin of the ECA (1.22%). In individual cadavers, the CS was located at the origin of the ICA in 97.6% on at least one side. The sites of the CS were asymmetrical in 34.1%.Conclusions: Clinicians performing carotid interventions should be aware of these anatomical variations to avoid inadvertent stimulation of the CS which can cause profound bradycardia and hypotension. [ABSTRACT FROM AUTHOR]

Background: Lipopolysaccharide (LPS) induces acute inflammation, activates sympathetic nerve activity (SNA) and alters hemodynamics. Since the arterial baroreflex is a negative feedback system to stabilize arterial pressure (AP), examining the arterial baroreflex function is a prerequisite to understanding complex hemodynamics under LPS challenge. We investigated the impact of LPS-induced acute inflammation on SNA and AP regulation by performing baroreflex open-loop analysis. Methods: Ten anesthetized Sprague-Dawley rats were used. Acute inflammation was induced by an intravenous injection of LPS (60 μg/kg). We isolated the carotid sinuses from the systemic circulation and controlled carotid sinus pressure (CSP) by a servo-controlled piston pump. We matched CSP to AP to establish the baroreflex closed-loop condition, whereas we decoupled CSP from AP to establish the baroreflex open-loop condition and changed CSP stepwise to evaluate the baroreflex open-loop function. We recorded splanchnic SNA and hemodynamic parameters under baroreflex open- and closed-loop conditions at baseline and at 60 and 120 min after LPS injection. Results: In the baroreflex closed-loop condition, SNA continued to increase after LPS injection, reaching three-fold the baseline value at 120 min (baseline: 94.7 ± 3.6 vs. 120 min: 283.9 ± 31.9 a.u.). In contrast, AP increased initially (until 75 min), then declined to the baseline level. In the baroreflex open-loop condition, LPS reset the neural arc (CSP-SNA relationship) upward to higher SNA, while shifted the peripheral arc (SNA-AP relationship) downward at 120 min after the injection. As a result, the operating point determined by the intersection between function curves of neural arc and peripheral arc showed marked sympatho-excitation without substantial changes in AP. Conclusions: LPS-induced acute inflammation markedly increased SNA via resetting of the baroreflex neural arc, and suppressed the peripheral arc. The balance between the augmented neural arc and suppressed peripheral arc determines SNA and hemodynamics in LPS-induced acute inflammation. [ABSTRACT FROM AUTHOR]

Background The number of patients with eosinophilic chronic rhinosinusitis (ECRS) has been increasing in recent years in Japan. In ECRS, nasal polyps recur immediately after endoscopic sinus surgery. The molecular biological mechanism underlying the refractoriness of ECRS is unclear. Methods Whole-transcriptome analysis with next-generation sequencing (RNA-seq) was conducted to investigate the molecular biological mechanism of ECRS. Real-time PCR, immunohistochemical staining, and immunofluorescence staining were performed to validate the results of RNA-seq. Results RNA-seq analysis revealed that in the nasal polyps of ECRS, the levels of 3 transcripts were elevated significantly and those of 7 transcripts were diminished significantly. Among the genes encoding these transcripts, TRPV3 (transient receptor potential cation channel, subfamily V, member 3) was identified as the only gene that is highly expressed in ECRS nasal polyps but this gene's expression was not previously detected using DNA microarray analysis in peripheral blood eosinophils. TRPV3 is newly identified here as a gene transcribed in ECRS. Our analysis also revealed that TRPV3 was highly expressed in the infiltrating eosinophils and mucosal epithelium of the nasal polyps of ECRS, and further that the more severe the refractoriness was after surgery, the higher the TRPV3 expression was in nasal polyps. Conclusions TRPV3 might play a role in the refractoriness of ECRS. Additional studies are required to evaluate the function of TRPV3 in ECRS. [ABSTRACT FROM AUTHOR]

The baroreceptors in the neck and aortic arch are important regulators of sudden blood pressure changes. They are innervated by CN IX and X and synapse in the brainstem. Baroreceptor failure is an under-recognized cause of recurrent syncope, orthostatic hypotension, and volatile hypertension, which is refractory to and may in fact worsen with conventional treatments. Baroreflex failure can be the result of neck and chest radiation, head and neck surgery, and cerebrovascular accidents involving the brainstem nuclei. The management of baroreflex failure is a challenge since patient education, lifestyle changes, and family support are extremely important in managing blood pressure. Leg exercises and Thrombo-Embolic Deterrent Stockings (TED) stockings are important in treating orthostatic hypotension. Clonidine is the antihypertensive of choice for supine hypertension. Low-dose benzodiazepines are helpful in suppressing sympathetic surges. We have encountered two patients with baroreflex failure after chemotherapy and radiation to the neck or upper chest. Temporal relationship between symptoms onset and the history of head, neck, and upper chest radiation or trauma is important in reaching a diagnosis.

We present a case of large multinodular goiter with retrosternal extension scheduled for thyroidectomy under general anesthesia (GA). We anticipated difficult airway due to tracheal compression as well as perioperative hemodynamic instability. She had had hyperthyroidism previously, which had been treated successfully. We planned and prepared to encounter airway problems in the light of Difficult Airway Society guidelines. After counselling and consent, her upper airways were sprayed with local anesthetic solution. Awake, flexible fiberoptic nasal intubation was performed and GA was induced. She had two episodes of bradycardia and hypotension peri-operatively, which were treated with inj atropine. Tracheostomy was performed in anticipation of tracheomalacia, which was de-cannulated on 3rd postoperative day. She was discharged on 4th post-operative day. [ABSTRACT FROM AUTHOR]