Carotid Body Ablation Research Articles

Effects of selective carotid body stimulation with adenosine in conscious humans.

In humans, excitation of peripheral chemoreceptors with systemic hypoxia causes hyperventilation, hypertension and tachycardia. However, the contribution of particular chemosensory areas (carotid vs. aortic bodies) to this response is unclear. We showed that selective stimulation of the carotid body by the injection of adenosine into the carotid artery causes a dose-dependent increase in minute ventilation and blood pressure with a concomitant decrease in heart rate in conscious humans. The ventilatory response was abolished and the haemodynamic response was diminished following carotid body ablation. We found that the magnitude of adenosine evoked responses in minute ventilation and blood pressure was analogous to the responses evoked by hypoxia. By contrast, opposing heart rate responses were evoked by adenosine (bradycardia) vs. hypoxia (tachycardia). Intra-carotid adenosine administration may provide a novel method for perioperative assessment of the effectiveness of carotid body ablation, which has been recently proposed as a treatment strategy for sympathetically-mediated diseases. Stimulation of peripheral chemoreceptors by acute hypoxia causes an increase in minute ventilation (VI), heart rate (HR) and arterial blood pressure (BP). However, the contribution of particular chemosensory areas, such as carotid (CB) vs. aortic bodies, to this response in humans remains unknown. We performed a blinded, randomized and placebo-controlled study in 11 conscious patients (nine men, two women) undergoing common carotid artery angiography. Doses of adenosine ranging from 4 to 512μg or placebo solution of a matching volume were administered in randomized order via a diagnostic catheter located in a common carotid artery. Separately, ventilatory and haemodynamic responses to systemic hypoxia were also assessed. Direct excitation of a CB with intra-arterial adenosine increased VI, systolic BP, mean BP and decreased HR. No responses in these variables were seen after injections of placebo. The magnitude of the ventilatory and haemodynamic responses depended on both the dose of adenosine used and on the level of chemosensitivity as determined by the ventilatory response to hypoxia. Percutaneous radiofrequency ablation of the CB abolished the adenosine evoked respiratory response and partially depressed the cardiovascular response in one participant. The results of the present study confirm the excitatory role of purines in CB physiology in humans and suggest that adenosine may be used for selective stimulation and assessment of CB activity. The trial is registered at ClinicalTrials.gov NCT01939912.

Carotid Body Ablation Abrogates Hypertension and Autonomic Alterations Induced by Intermittent Hypoxia in Rats.

Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, enhances carotid body (CB) chemosensory responses to hypoxia and produces autonomic dysfunction, cardiac arrhythmias, and hypertension. We tested whether autonomic alterations, arrhythmogenesis, and the progression of hypertension induced by CIH depend on the enhanced CB chemosensory drive, by ablation of the CB chemoreceptors. Male Sprague-Dawley rats were exposed to control (Sham) conditions for 7 days and then to CIH (5% O2, 12/h 8 h/d) for a total of 28 days. At 21 days of CIH exposure, rats underwent bilateral CB ablation and then exposed to CIH for 7 additional days. Arterial blood pressure and ventilatory chemoreflex response to hypoxia were measured in conscious rats. In addition, cardiac autonomic imbalance, cardiac baroreflex gain, and arrhythmia score were assessed during the length of the experiments. In separate experimental series, we measured extracellular matrix remodeling content in cardiac atrial tissue and systemic oxidative stress. CIH induced hypertension, enhanced ventilatory response to hypoxia, induced autonomic imbalance toward sympathetic preponderance, reduced baroreflex gain, and increased arrhythmias and atrial fibrosis. CB ablation normalized blood pressure, reduced ventilatory response to hypoxia, and restored cardiac autonomic and baroreflex function. In addition, CB ablation reduced the number of arrhythmias, but not extracellular matrix remodeling or systemic oxidative stress, suggesting that reductions in arrhythmia incidence during CIH were related to normalization of cardiac autonomic balance. Present results show that autonomic alterations induced by CIH are critically dependent on the CB and support a main role for the CB in the CIH-induced hypertension.

Device-based Therapy for Hypertension.

Hypertension continues to be a major contributor to global morbidity and mortality, fuelled by an abundance of patients with uncontrolled blood pressure despite the multitude of pharmacological options available. This may occur as a consequence of true resistant hypertension, through an inability to tolerate current pharmacological therapies, or non-adherence to antihypertensive medication. In recent years, there has been a rapid expansion of device-based therapies proposed as novel non-pharmacological approaches to treating resistant hypertension. In this review, we discuss seven novel devices—renal nerve denervation, baroreflex activation therapy, carotid body ablation, central iliac arteriovenous anastomosis, deep brain stimulation, median nerve stimulation, and vagal nerve stimulation. We highlight how the devices differ, the varying degrees of evidence available to date and upcoming trials. This review also considers the possible factors that may enable appropriate device selection for different hypertension phenotypes.

From the Cover: Prenatal Nicotinic Exposure Attenuates Respiratory Chemoreflexes Associated With Downregulation of Tyrosine Hydroxylase and Neurokinin 1 Receptor in Rat Pup Carotid Body.

Maternal cigarette smoke is the major risk of sudden infant death syndrome (SIDS). A depressed ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) is thought to be responsible for the pathogenesis of SIDS and the carotid body is critically involved in these responses. We have recently reported that prenatal nicotinic exposure (PNE) over the full gestation induces depressed HVR in rat pups. Here, we asked whether PNE (1) depressed not only HVR but also HCVR that were dependent on the carotid body, (2) affected some important receptors and neurochemicals expressed in the carotid body, such as tyrosine hydroxylase (TH), neurokinin-1 receptor (NK1R), and α7 nicotinic acetylcholine receptor (α7nAChR), and (3) blunted the ventilatory responses to activation of these receptors. To this end, HVR and HCVR in Ctrl and PNE pups were measured with plethysmography before and after carotid body ablation (Series I), mRNA expression and/or immunoreactivity (IR) of TH, NK1R, and α7nAChR in the carotid body were examined by RT-PCR and immunohistochemistry (Series II), and the ventilatory responses were tested before and after intracarotid injection of substance P (NK1R agonist) and AR-R17779 (α7nAChR agonist) (Series III). Our results showed that PNE (1) significantly depressed both HVR and HCVR and these depressions were abolished by carotid body ablation, (2) reduced the relative population of glomus cells, mRNA NK1R, and α7nAChR and IR of NK1R and TH in the carotid body, and (3) decreased ventilatory responses to intracarotid injection of substance P or AR-R17779. These results suggest that PNE acting via the carotid body could strikingly blunt HVR and HCVR, likely through downregulating TH and NK1R.

Carotid body ablation in heart failure: A new pathway for rescuing autonomic balance

Carotid body ablation in heart failure: A new pathway for rescuing autonomic balance

Carotid Body Ablation Reverses the Hypertension and Autonomic Changes Induced by Intermittent Hypoxia

Chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea syndrome, enhances carotid body (CB) chemosensory discharges in normoxia, eliciting sympathetic overactivation and hypertension. We propose that the enhanced CB chemosensory drive plays a crucial role in the generation of the hypertension during CIH. To study the origin of higher blood pressures during CIH, we performed selective ablation of the CB once animals became hypertensive following CIH exposure. Male Sprague‐Dawley rats (200 g) were exposed to CIH (5% O2, 12 times/h, 8 h/day) and arterial blood pressure (BP) was measured with radiotelemetry. After 3 weeks of CIH, under anesthesia both CBs were cryogenically destroyed with an ice cold needle, and rats were kept one more week in CIH. The effectiveness of this maneuver was confirmed by the disappearance of the ventilatory response to NaCN. After 3 weeks of CIH exposure, rats displayed hypertension (BP~10 mmHg), enhanced hypoxic ventilatory response and reduced baroreflex sensitivity (BRS) from 2.28±0.05 to 1.76±0.10 ms/mmHg. The ablation of the CBs markedly decreases the elevated BP, reduced the enhanced ventilatory response to hypoxia and normalized BRS to 2.52±0.12 ms/mmHg. We found that the cardiorespiratory alterations induced by CIH are critically dependent on functional CB chemoreceptors. Also, our results showed that the CIH‐induced hypertension was abolished by ablation of the CB despite the continuous exposure to CIH stimulation. Thus, our results indicate that the CB plays a pivotal role in the progression and maintenance of the CIH‐induced hypertension.Supported by Puente 28/2014 PUC

New approaches in the treatment of hypertension.

Hypertension is the most common modifiable risk factor for cardiovascular disease and death, and lowering blood pressure with antihypertensive drugs reduces target organ damage and prevents cardiovascular disease outcomes. Despite a plethora of available treatment options, a substantial portion of the hypertensive population has uncontrolled blood pressure. The unmet need of controlling blood pressure in this population may be addressed, in part, by developing new drugs and devices/procedures to treat hypertension and its comorbidities. In this Compendium Review, we discuss new drugs and interventional treatments that are undergoing preclinical or clinical testing for hypertension treatment. New drug classes, eg, inhibitors of vasopeptidases, aldosterone synthase and soluble epoxide hydrolase, agonists of natriuretic peptide A and vasoactive intestinal peptide receptor 2, and a novel mineralocorticoid receptor antagonist are in phase II/III of development, while inhibitors of aminopeptidase A, dopamine β-hydroxylase, and the intestinal Na(+)/H(+) exchanger 3, agonists of components of the angiotensin-converting enzyme 2/angiotensin(1-7)/Mas receptor axis and vaccines directed toward angiotensin II and its type 1 receptor are in phase I or preclinical development. The two main interventional approaches, transcatheter renal denervation and baroreflex activation therapy, are used in clinical practice for severe treatment resistant hypertension in some countries. Renal denervation is also being evaluated for treatment of various comorbidities, eg, chronic heart failure, cardiac arrhythmias and chronic renal failure. Novel interventional approaches in early development include carotid body ablation and arteriovenous fistula placement. Importantly, none of these novel drug or device treatments has been shown to prevent cardiovascular disease outcomes or death in hypertensive patients.

Mechanisms of carotid body chemoreflex dysfunction during heart failure.

What is the topic of this review? Carotid body chemoreceptor activity is tonically elevated in heart failure and contributes to morbidity due to the reflex activation of sympathetic nerve activity and destabilization of breathing. The potential causes for the enhanced chemoreceptor activation in heart failure are discussed. What advances does it highlight? The role of a chronic reduction in blood flow to the carotid body due to cardiac failure and its impact on signalling pathways in the carotid body is discussed. Recent advances have attracted interest in the potential for carotid body (CB) ablation or desensitization as an effective strategy for clinical treatment and management of cardiorespiratory diseases, including hypertension, heart failure, diabetes mellitus, metabolic syndrome and renal failure. These disease states have in common sympathetic overactivity, which plays an important role in the development and progression of the disease and is often associated with breathing dysregulation, which in turn is likely to mediate or aggravate the autonomic imbalance. Evidence from both chronic heart failure (CHF) patients and animal models indicates that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in sympathetic activity and the development of periodic breathing associated with the disease. Although this maladaptive change is likely to derive from altered function at all levels of the reflex arc, a tonic increase in afferent activity from CB glomus cells is likely to be a main driving force. This report focuses on our understanding of mechanisms that alter CB function in CHF and their potential translational impact on treatment of CHF.

Selective carotid body ablation in experimental heart failure: a new therapeutic tool to improve cardiorespiratory control.

What is the topic of this review? This review summarizes the physiological role played by the carotid body in the autonomic dysregulation and breathing disturbances during the progression of chronic heart failure and the therapeutic potential of carotid body ablation to control cardiorespiratory imbalance and improve survival in heart failure. What advances does it highlight? Carotid body ablation markedly improves breathing stability and normalizes autonomic function in chronic heart failure. More importantly, if carotid body ablation is performed early during the progression of the disease it significantly improves animal survival. Chronic heart failure (CHF) is a leading medical problem worldwide. Common hallmarks of CHF include autonomic imbalance and breathing disorders, both of which are closely related to the progression of the disease and strongly predict mortality in CHF patients. The role played by the carotid body (CB) chemoreceptors in the progression of CHF has received attention because enhanced carotid chemoreflex drive is thought to contribute to autonomic dysfunction, abnormal breathing patterns and increased mortality in CHF. Therefore, therapeutic tools intended to normalize CB-mediated chemoreflex drive could have the potential to improve quality of life and decrease mortality of CHF patients. In experimental CHF, an enhancement of the CB chemoreflex drive, elevated sympathetic outflow, increased resting breathing variability, increased incidence of apnoea and desensitization of the baroreflex have been shown. Notably, selective elimination of the CB reduced central presympathetic neuronal activation, normalized sympathetic outflow and baroreflex sensitivity and stabilized breathing function in CHF. More remarkably, CB ablation has been shown to be a valuable therapeutic tool that significantly reduced aberrant cardiac remodelling, improved left ventriclular ejection fraction and reduced cardiac arrhythmogenesis. Most importantly, animals with CHF that underwent CB ablation showed a marked improvement in survival rate. Interestingly, a case report from a heart failure patient in whom unilateral CB ablation was performed showed promising results, with significant improvement in autonomic balance and breathing variability. Together, the CHF data from experimental animals as well as humans unveil a major role for the CB chemoreceptors in the progression of heart failure and support the notion that CB ablation could represent a novel therapeutic strategy to reduce cardiorespiratory dysfunction and improve survival during heart failure.

Update on interventional approaches to treatment of hypertension

In spite of availability of numerous drug treatments for arterial hypertension (HTN), there is a need for new approaches, especially in case of treatment-resistant forms. Available new interventional methods for HTN are briefly reviewed with focus on approaches in early stages of development beyond the most studied and discussed renal denervation: baroreflex activation therapy, carotid body ablation, arteriovenous fistula, neurovascular decompression, deep brain stimulation and spinal cord stimulation. Most of these approaches affect blood pressure level through modulation of autonomous nervous system activity. Some of them (e. g. renal denervation and baroreflex activation therapy) are modern technical modification of the methods which were used to treat HTN in the past century. Other methods (e.g. deep brain stimulation, spinal cord stimulation, arteriovenous fistula) were under development for other indications. All of these approaches are still far away from implementation in routine clinical practice. Further investigations of safety and efficacy in the randomized clinical studies are warranted together with technical optimization and definition of patients’ subgroup who will benefit from precise approach together with efficacy criteria and predictors.

Crucial Role of the Carotid Body Chemoreceptors on the Development of High Arterial Blood Pressure During Chronic Intermittent Hypoxia.

Exposure to chronic intermittent hypoxia (CIH), the main feature of obstructive sleep apnea, produces autonomic and cardiorespirartory alterations, and leads to systemic hypertension. These alterations are associated with enhanced carotid body (CB) chemosensory and ventilatory hypoxic reflexes and a decrease baroreflex (BRS) efficiency. The aim of this study was to determine the therapeutic effect of CB ablation on the elevated arterial blood pressure, the reduced BRS and the potentiated ventilatory response induced by CIH in conscious rats. Arterial blood pressure (BP) was continuous measured by telemetry in male Sprague-Dawley rats exposed to CIH (5 % O(2), 12 times/h, and 8 h/day). After 21 days of CIH, the CBs were selectively cryodestroyed, and rats were kept one more week in CIH. Ventilatory responses to hypoxia were assessed by whole body plethysmography and spontaneous BRS measured by the sequence method. Exposure to CIH produces hypertension, increased the chemoreflex ventilatory hypoxic responses, and decreased BRS. The ablation of the CBs normalized the elevated BP, and the altered ventilatory response and BRS. Present results suggest that the CB play a crucial role in the development of high arterial pressure and autonomic alterations induced by CIH.

Coping with acute hypertensive stressors after selective carotid body ablation in conscious spontaneously hypertensive rats (873.10)

We have previously shown that bilateral carotid sinus denervation in SHR reduces arterial pressure (AP). This technique, however, also removes carotid sinus baroreceptors. We hypothesized that the fall in basal AP with selective bilateral CBA would not impair the normal cardiovascular responses to hypoxia, exercise and restraint stress. SHR were implanted with telemetry devices to record AP, and responses to hypoxia (10% O2), exercise (10m/min) and restraint stress were tested. The chemoreflex was tested with i.v. sodium cyanide (120μg.kg‐1); this response was abolished after CBA (n=4) but preserved in Shams (n=3). Basal systolic AP fell significantly after 14 days in CBA (‐18.2±2mmHg) compare to Sham (2.5±0.6mmHg), (P<0.05). SHR with CBA showed a depressor effect to 10% oxygen (‐15.3±7mmHg) whereas a pressor response was seen in Sham (15.9±6mmHg; P<0.029); heart and respiratory rates were not different. The change in AP was similar between groups during both exercise (CBA 12±7 vs. Sham 23±8mmHg, respectively; NS) and restraint stress (CBA 28±8 vs. Sham 17±9mmHg; NS). We conclude that chronic CBA prevents the pressor response to hypoxia but does not affect cardiovascular adjustment to exercise and restraint stress.Grant Funding Source: Supported by the British Heart Foundation and Cibiem

Carotid Chemoreceptor Ablation Improves Survival in Heart Failure: Rescuing Autonomic Control of Cardiorespiratory Function

This study sought to investigate whether selective ablation of the carotid body (CB) chemoreceptors improves cardiorespiratory control and survival during heart failure. Chronic heart failure (CHF) is a recognized health problem worldwide, and novel treatments are needed to better improve life quality and decrease mortality. Enhanced carotid chemoreflex drive from the CB is thought to contribute significantly to autonomic dysfunction, abnormal breathing patterns, and increased mortality in heart failure. Chronic heart failure was induced by coronary ligation in rats. Selective CB denervation was performed to remove carotid chemoreflex drive in the CHF state (16 weeks post-myocardial infarction). Indexes of autonomic and respiratory function were assessed in CB intact and CB denervated animals. CB denervation at 2 weeks post-myocardial infarction was performed to evaluate whether early targeted CB ablation decreases the progression of left ventricular dysfunction, cardiac remodeling, and arrhythmic episodes and improves survival. The CHF rats developed increased CB chemoreflex drive and chronic central pre-sympathetic neuronal activation, increased indexes of elevated sympathetic outflow, increased breathing variability and apnea incidence, and desensitization of the baroreflex. Selective CB ablation reduced the central pre-sympathetic neuronal activation by 40%, normalized indexes of sympathetic outflow and baroreflex sensitivity, and reduced the incidence of apneas in CHF animals from 16.8 ± 1.8 events/h to 8.0 ± 1.4 events/h. Remarkably, when CB ablation was performed early, cardiac remodeling, deterioration of left ventricle ejection fraction, and cardiac arrhythmias were reduced. Most importantly, the rats that underwent early CB ablation exhibited an 85% survival rate compared with 45% survival in CHF rats without the intervention. Carotid chemoreceptors play a seminal role in the pathogenesis of heart failure, and their targeted ablation might be of therapeutic value to reduce cardiorespiratory dysfunction and improve survival during CHF.

Restoring autonomic balance: future therapeutic targets

Our aim was to highlight the very recent and rapid expansion of a number of contemporary, pioneering and projected interventional approaches for resistant hypertension. Our discussions of each approach centre on a new model of the cardiovascular system that emphasises the importance of the sympathetic nervous system, its differential control and reflex activation. Four interventional therapeutic strategies are discussed including targeted sympathectomies and carotid body ablation. Harnessing endogenous homeostatic control systems looks promising as a means to correct autonomic balance. The challenge will be in deciding which interventional approach should be selected.

Carotid body ablation improves survival, breathing disorders and autonomic control in heart failure rats

Sympathetic hyperactivity and breathing instability contribute to decompensation during chronic heart failure (CHF). Enhanced carotid body (CB) chemoreflex drive has been related to increased sympathetic outflow and breathing disorders in CHF. We hypothesized that ablation of CB afferents (CBA) improves cardiorespiratory function and survival in CHF. Selective CBA was performed on male Sprague‐Dawley rats after 16 weeks (wk) of coronary artery ligation (EF < 45%). Resting breathing and ventilatory responses to acute hypoxia (FiO2‐10%) were measured by plethysmography prior to and one wk after CBA/sham surgery. Heart rate (HRV) and systolic blood pressure variability (BPV) and spontaneous baroreflex gain (BG) were similarly determined at rest. Neuronal activation was assessed in the rostral ventrolateral medulla (RVLM) at the end of the study using Fra‐1 expression. CHF rats compared to sham exhibited elevated apnea incidence, hypoxic ventilatory responses, LF/HF HRV, LF‐BPV, and RVLM Fra‐1 expression and decreased BG. CBA in CHF rats decreased (pre‐ vs. post‐CBA, P < .05), LF/HF HRV (2.1±0.3 vs. 0.9±0.2), LF‐BPV (18.4±4.5 vs. 7.2±2.0 mmHg2), apnea frequency (16.8±1.8 vs. 10.6±0.6 events/h), RVLM Fra‐1 expression (1.5±0.1 vs. 0.9±0.1 a.u.), and increased BG (1.0±0.1 vs. 1.9±0.3 ms/mmHg) to levels comparable to sham rats. Mortality rate at 16 wk post infarct was elevated in CHF compared to sham (33% vs. 7%). CBA at 2 wk post infarct reduced the mortality rate in CHF rats at 16 wk to 15%. Our results show that CBA reduces hyperactivation of the RVLM and improves cardiorespiratory control and survival in CHF rats. Supported by NIH PO1‐HL62222.

Retrotrapezoid nucleus lesions decrease phrenic activity and CO 2 sensitivity in rats

In chloralose-urethane anesthetized, paralyzed, and ventilated rats, we measured the effects of unilateral lesions in the region ventral and ventromedial to the facial nucleus, the retrotrapezoid nucleus (RTN), on eucapnic phrenic activity and the response to increased end-tidal CO 2. Chemical (kainic acid injections; 4.7 mM; 10–100 nl) and electrolytic (5–15 mA; 5–15 sec) lesions, anatomically demonstrated to be in the RTN, resulted in a progressive decrease in the amplitude of the integrated phrenic nerve activity from baseline levels of 49–59% of maximum to values of 21–32% of maximum over 30 to 120 min. There were no consistent effects on frequency or on blood pressure. The initial slope of the response to hypercapnia was decreased by 86–92%. Bilateral carotid body ablation did not alter the general pattern of the responses. As in the cat, unilateral RTN lesions decrease baseline phrenic amplitude and virtually abolish the response to hypercapnia. We hypothesize that the RTN region provides; (1) a source of tonic activity which maintains eucapnic ventilatory output, and (2) allows expression of the response to hypercapnia.

Responses of respiratory modulated and tonic units in the retrotrapezoid nucleus to CO 2

We hypothesized that the retrotrapezoid nucleus (RTN) contains both respiratory modulated (RM) and non-respiratory modulated (NRM) neurons which participate in the ventilatory response to increased CO 2. We made extracellular recordings of the activity of 46 single units in the RTN of 9 decerebrate, paralyzed, ventilated cats (5 intact; 4 with carotid body and sinus ablation) under eucapnic (P CO2 = 34.2±3.5 mmHg; mean ± SD) and hypercapnic (P CO2 = 47.4 ± 3.4 mmHg) conditions. To define a RM unit, we used the η 2 statistic which is the ratio of the variance of the unit firing rate within respiratory cycles to that across respiratory cycles. We classified the units of RM ( N=17) if the η 2 values in eucapnia or hypercapnia were ≥0.25 and as NRM ( N=29) if the values were <0.25. Overall, 19/46 units (41%) increased their firing rate with increased CO 2, 5 decreased their firing rate, and 22 had no significant change in firing rate. Of 17 RM units, 8 (47%) increased their mean firing rate with hypercapnia from 7.6±3.9 to 23.2±6.8 spikes/sec. These included 5 inspiratory units, 2 inspiratory units that had an onset of firing in late expiration (Pre-I/I), and 1 expiratory unit. Seven of these also changed their discharge pattern (eucapnic η 2=0.02 to 0.12; hypercapnic η 2=0.34 to 0.79) of 29 NRM units 11 (38%) showed a significant increase in mean firing rate with CO 2 stimulation from 19.8±7.2 to 31.3±82. spikes/sec. The RTN has RM units which change their discharge pattern and firing rate in response to increased CO 2, as do units within the medulla and pons, and it has NRM units which are also responsive to increased CO 2. These data indicate that some neurons of the RTN are involved in the central chemoreceptor response but they provide no direct evidence that chemoreception resides within the RTN.

Influence of carotid body ablation on erythropoietin production in rabbits.

ARTICLESInfluence of carotid body ablation on erythropoietin production in rabbitsLG Paulo, GD Fink, BL Roh, and JW FisherLG Paulo, GD Fink, BL Roh, and JW FisherPublished Online:01 Feb 1973https://doi.org/10.1152/ajplegacy.1973.224.2.442MoreSectionsPDF (744 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByOlfactory receptor 78 regulates erythropoietin and cardiorespiratory responses to hypobaric hypoxiaBenjamin Wang,* Ying-Jie Peng,* Xiaoyu Su, Chongxu Zhang, Jason S. Nagati, Joseph A. Garcia, and Nanduri R. Prabhakar16 April 2021 | Journal of Applied Physiology, Vol. 130, No. 4Chapter 1 Trophic Factors in the Carotid BodyErythropoietin regulates hypoxic ventilation in mice by interacting with brainstem and carotid bodies24 October 2005 | The Journal of Physiology, Vol. 568, No. 2Reflex Responses to Chemoreceptor Stimulation1 January 2011The innervation of glomus cells, ganglion cells and blood vessels in the rat carotid body: A quantitative ultrastructural analysisJournal of Neurocytology, Vol. 4, No. 2Hereditary tumors of the carotid bodies and chronic obstructive pulmonary diseaseCancer, Vol. 33, No. 6Renal erythropoietin: Properties and production More from this issue > Volume 224Issue 2February 1973Pages 442-444 Copyright & PermissionsCopyright © 1973 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1973.224.2.442PubMed4686500History Published online 1 February 1973 Published in print 1 February 1973 Metrics

Enhancement of the erythropoietic response of cats to hypoxia following removal of the carotid body.

SummaryPlasma erythropoietin levels in carotid body-ablated cats exposed to hypoxia (0.50 atm for 18 hr) 48 hr after removal of the carotid bodies were significantly higher than that of sham-operated controls exposed to the same degree of hypoxia. The mean plasma ESF levels in the carotid body-ablated group (1.29 ± 0.16 units/ml of plasma) were significantly (p < 0.05) higher than that of sham-operated controls (0.74 ± 0.11 units/ml of plasma). However, plasma ESF levels in cats exposed to hypoxia 2 wk after carotid body ablation or sham-operation were not significantly different. The present studies indicate that removal of the carotid bodies in cats enhances the erythropoietic response to hypoxia.