Bilateral Carotid Body Resection Research Articles

Oxygenation pattern and compensatory responses to hypoxia and hypercapnia following bilateral carotid body resection in humans.

Five years after bilateral carotid body resection (bCBR) performed in four patients, the absence of the hypoxic ventilatory response persisted, suggesting no compensatory regrowth. Breathing hypoxic gas mixtures (15% and 12%) results in a lower (by ∼10%) minimal blood oxygen saturation ( ) in bCBR patients compared to heart failure subjects (CHF) with intact peripheral chemoreceptors. After bCBR, patients were characterized by a greater short-term variability in during mild hypoxia in comparison to the CHF group. The ventilatory response to hypercapnia was preserved following bCBR and was sufficient to maintain minimal at levels comparable to controls when combined with hypoxia. Bilateral CBR - a novel treatment modality for sympathetically mediated diseases - should be used with caution due to the risk of significant desaturation even during mild hypoxia equivalent to that experienced during long-haul air travel and high altitude. Carotid body resection has been proposed as a novel treatment for sympathetically mediated diseases but the safety of bilateral carotid body resection (bCBR) for blood oxygenation during hypoxic stress (long-haul flights or high altitude) remains uncertain. Also unknown is whether central ventilatory drive is sufficient to maintain adequate oxygen saturation when exposed to hypercapnia with concomitant hypoxia. Thus, we administered: 15% O2 , 12% O2 , 5% CO2 /12% O2 and 5% CO2 /95% O2 to a group of four patients with congestive heart failure (65±2.9years) in whom bCBR was performed 5years earlier. Ventilatory, haemodynamic and blood oxygen saturation ( ) responses were recorded non-invasively and compared to control groups with intact peripheral chemoreceptors (both healthy and heart failure patients). First, we confirmed that the ventilatory response to hypoxia was eliminated in patients with bCBR, although the increase in cardiac output was preserved. Second, administration of hypoxic gas mixtures resulted in a larger decrease in and greater short-term variability of the leading to a lower minimal for both hypoxia levels in the bCBR group compared to heart failure controls (82.5±1.2% vs. 91.6±2.3% for 15% O2 and 73.8±4.0% vs. 83.7±3.1% for 12% O2 ). Third, in bCBR patients the ventilatory response to hypercapnia was present and sufficient to maintain a minimal at a level comparable to heart failure controls following administration of 5% CO2 /12% O2 (88.7±4.2% vs. 91.1±2.8%). We conclude that bCBR carries a risk of significant oxygen desaturation even during mild hypoxia. Despite preservation of central chemosensitivity, future studies should focus on unilateral CBR or on pharmacological modulation of peripheral chemosensitivity.

DON’T FORGET TO BREATHE: A CASE OF HYPOXEMIA AFTER CAROTID BODY RESECTION

SESSION TITLE: Pulmonary Physiology SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Carotid body tumors (CBTs) are paragangliomas, slow-growing neuroendocrine tumors that secrete catecholamines. Management involves surgical resection or radiation. Although chronic hypoxia has been identified after resection of these tumors, the effects of altitude on oxygenation in these patients has not been well-described. We present a case of chronic hypoxia in a patient after bilateral CBT resection. CASE PRESENTATION: A 72 year-old male with a personal and family history of bilateral CBTs presented for evaluation of hypoxia. He underwent resection of these tumors one year prior to presentation. Final tissue exam identified benign carotid body paragangliomas. He had a significant history of tobacco use but had quit 5 years prior. Given his new hypoxia, he underwent evaluation for COPD. Review of systems was notable for dyspnea with heavy exertion but he was otherwise without respiratory complaints. He lived at 1200m above sea level without significant dyspnea, but frequently traveled to 2500m above sea level where his dyspnea would worsen. On exam his baseline SpO2 was 90-91%, but increased quickly to 97-98% with frequent deep breaths. Due to concern for COPD, pulmonary function testing (PFT), plethysmography and DLCO were obtained and all normal. 6MWT was significant for desaturations that improved with 2-3L/min of supplemental O2. ABG showed minimal hypoventilation with a PaCO2 42mm Hg at rest. Overnight oximetry showed mild sustained hypoxemia. CT chest, PET and a V/Q scan were obtained and were all unremarkable. The patient was started on 2-3L/min of supplemental O2 with ambulation and sleep. At one year follow-up he reported control of his dyspnea even at high altitudes. DISCUSSION: The effects of ventilatory control in patients after bilateral carotid-body resection has been previously described. It is theorized that the carotid bodies are responsible for the hyperpnea that results from hypoxia; the aortic chemoreceptors to a much lesser extent. Brainstem respiratory centers receive afferent impulses from the carotid bodies during hypoxia and hypercapnia to control ventilation by increasing MV. In those who have undergone bilateral carotid body resection, there is minimal to no change in MV during hypoxia. At altitudes higher than 2000m the atmospheric O2 pressure decreases causing chronic hypoxia. This case demonstrates the effects of this reduced atmospheric O2 pressure in a patient that has undergone a bilateral carotid body resection. CONCLUSIONS: Providers should be aware that in patients who have undergone carotid body resection, regulatory control of ventilation is impaired, resulting in diminished increase in MV response to hypoxia. At higher altitudes, this becomes clinically significant due to the reduced atmospheric O2 pressure inspired. Patients with hypoxia after bilateral carotid body resections should be advised to use supplementary O2, especially at high altitudes. Reference #1: Erickson et al. “Benign Paragangliomas.” J Clin Endocrinol Metab. 2001 Nov; 86 (11): 5210-5216. Reference #2: Lugliani et al. “Effect of bilateral carotid-body resection on ventilatory control at rest and during exercise in man,” The New England Journal of Medicine. 1971; 285 (20):1105–1111. Reference #3: Rodríguez-Cuevas et al. "Carotid body tumors in inhabitants of altitudes higher than 2000 meters above sea level.” Head & Neck. 1998; 20:374-378. DISCLOSURES: No relevant relationships by David Dorsey, source=Web Response No relevant relationships by Brian Foster, source=Web Response

Effect of Bilateral Carotid Body Resection on Cardiac Baroreflex Control of Blood Pressure During Hypoglycemia

Hypoglycemia results in a reduction in cardiac baroreflex sensitivity and a shift in the baroreflex working range to higher heart rates. This effect is mediated, in part, by the carotid chemoreceptors. Therefore, we hypothesized hypoglycemia-mediated changes in baroreflex control of heart rate would be blunted in carotid body-resected patients when compared with healthy controls. Five patients with bilateral carotid body resection for glomus tumors and 10 healthy controls completed a 180-minute hyperinsulinemic, hypoglycemic (≈3.3 mmol/L) clamp. Changes in heart rate, blood pressure, and spontaneous cardiac baroreflex sensitivity were assessed. Baseline baroreflex sensitivity was not different between groups (P>0.05). Hypoglycemia resulted in a reduction in baroreflex sensitivity in both the groups (main effect of time, P<0.01) and responses were lower in resected patients when compared with controls (main effect of group, P<0.05). Hypoglycemia resulted in large reductions in systolic (-17±7 mm Hg) and mean (-14±5 mm Hg) blood pressure in resected patients that were not observed in controls (interaction of group and time, P<0.05). Despite lower blood pressures, increases in heart rate with hypoglycemia were blunted in resected patients (interaction of group and time, P<0.01). Major novel findings from this study demonstrate that intact carotid chemoreceptors are essential for increasing heart rate and maintaining arterial blood pressure during hypoglycemia in humans. These data support a contribution of the carotid chemoreceptors to blood pressure control and highlight the potential widespread effects of carotid body resection in humans.

P2X3 Receptor Antagonism Reduces Peripheral Chemoreceptor Reflex Hypersensitivity and Blood Pressure in the Spontaneously Hypertensive Rat

Arterial hypertension is associated with increased peripheral chemoreceptor reflex sensitivity. We have shown that bilateral carotid body (CBR) resection in spontaneously hypertensive (SH) rats reduces arterial pressure (AP). Since ATP is a major participant in CB transduction signalling, and P2X3 receptors are associated with visceral afferent sensitisation, we hypothesized that P2X3 antagonism would reduce chemoreflex hypersensitivity and lower AP in SH rats.SH and Wistar rats were implanted with telemeters to record AP. Doses of a P2X3 receptor antagonist (AF‐219) were administered as an i.v. bolus: 0.5 (n=4), 1 (n=4), 2 (n=5), 4 (n=5) and 8 mg/kg (n=4), and changes in both basal AP and chemoreflex sensitivity assessed. The chemoreflex was stimulated with sodium cyanide (NaCN; 120 μg/kg i.v.).At all doses, AF‐219 diminished NaCN evoked AP responses (P=0.084) in SH rats. In SH rats, basal AP was reduced by AF‐219 (P&lt;0.05): ‐8±3 mmHg, 0.5mg/kg; ‐16±1 mmHg, 1mg/kg: ‐18±3 mmHg, 2mg/kg; ‐13±1 mmHg, 4mg/kg; ‐13±2 mmHg, 8mg/kg. In normotensive Wistars, AF‐219 did not reduce AP vs. baseline (‐4±2 mmHg, 1 mg/kg; P&gt;0.05). Injections of vehicle had no effect in either rat strain (n=4). In SH rats, CBR blunted the 1 mg/kg AF‐219 induced fall in AP vs. non‐CBR rats. However, the fall versus baseline in AP in SH‐CBR rats remained significant (‐8±1 mmHg,P&lt;0.01).P2X3 receptor antagonism depresses chemoreflex hypersensitivity and lowers AP in SH rats to a level observed after selective CBR. P2X3 receptor antagonism may provide a novel way to attenuate CB tonicity in SH rats and as such become a novel target for controlling hypertension.Supported by: British Heart Foundation and the NIH

Effect of Carotid Body Resection on Baroreflex Control of Blood Pressure During Hypoglycemia

BackgroundHypoglycemia results in a reduction in spontaneous cardiac baroreflex sensitivity (scBRS) and a shift in the baroreflex working range to higher heart rates; this effect may be mediated by the carotid chemoreceptors. We hypothesized changes in baroreflex control of heart rate with hypoglycemia would be blunted in carotid body resected patients when compared with healthy controls.MethodsFive patients (3M/2F) with bilateral carotid body resection for glomus tumors and ten healthy controls (7M/3F) completed a 180‐min hyperinsulinemic, hypoglycemic (~3.3 µmol/mL) clamp. Changes in heart rate, blood pressure, and scBRS were assessed.ResultsscBRS was reduced from baseline during hypoglycemia (p&lt;0.01) and was lower in carotid body resected patients when compared with controls (p=0.01). Hypoglycemia‐mediated reductions in systolic and mean blood pressure were significantly greater in patients when compared with controls (p&lt;0.05). Despite lower blood pressures, increases in heart rate with hypoglycemia were blunted in patients (p&lt;0.01).ConclusionReductions in scBRS with hypoglycemia cannot be exclusively attributed to the carotid chemoreceptors; however, the chemoreceptors play a role in resetting the baroreflex working range to higher heart rates during hypoglycemia such that a rise in heart rate is not observed in carotid body resected patients. These data support a contribution of the carotid chemoreceptors to baroreflex control of blood pressure during hypoglycemia and highlight potential widespread effects of carotid body resection in humans.FundingDK090541, HL120570

Effect of bilateral carotid body resection on the counterregulatory response to hypoglycaemia in humans.

What is the central question of this study? Hyperoxia blunts hypoglycaemia counterregulation in healthy adults. We hypothesized that this effect is mediated by the carotid bodies and that: (i) hyperoxia would have no effect on hypoglycaemia counterregulation in carotid body-resected patients; and (ii) carotid body-resected patients would exhibit an impaired counterregulatory response to hypoglycaemia. What is the main finding and its importance? Our data indicate that the effect of hyperoxia on hypoglycaemic counterregulation is mediated by the carotid bodies. However, a relatively normal counterregulatory response to hypoglycaemia in carotid body-resected patients highlights: (i) the potential for long-term adaptations after carotid body resection; and (ii) the importance of redundant mechanisms in mediating hypoglycaemia counterregulation. Hyperoxia reduces hypoglycaemia counterregulation in healthy adults. We hypothesized that this effect is mediated by the carotid bodies and that: (i) hyperoxia would have no effect on hypoglycaemia counterregulation in patients with bilateral carotid body resection; and (ii) carotid body-resected patients would exhibit an impaired counterregulatory response to hypoglycaemia. Five patients (three male and two female) with bilateral carotid body resection for glomus tumours underwent two 180 min hyperinsulinaemic, hypoglycaemic (∼ 3.3 mmol l(-1)) clamps separated by a minimum of 1 week and randomized to either normoxia (21% fractional inspired O2 ) or hyperoxia (100% fractional inspired O2). Ten healthy adults (seven male and three female) served as control subjects. Hypoglycaemia counterregulation in carotid body-resected patients was not significantly altered by hyperoxia (area under the curve expressed as a percentage of the normoxic response: glucose infusion rate, 111 ± 10%; cortisol, 94 ± 6%; glucagon, 107 ± 7%; growth hormone, 92 ± 10%; adrenaline, 89 ± 26%; noradrenaline, 79 ± 15%; main effect of condition, P > 0.05). This is in contrast to previously published results from healthy adults. However, the counterregulatory responses to hypoglycaemia during normoxia were not impaired in carotid body-resected patients when compared with control subjects (main effect of group, P > 0.05). Our data provide further corroborative evidence that the effect of hyperoxia on hypoglycaemic counterregulation is mediated by the carotid bodies. However, relatively normal counterregulatory responses to hypoglycaemia in carotid body-resected patients highlight the importance of redundant mechanisms in mediating hypoglycaemia counterregulation.

Plasticity of Central Chemoreceptors: Effect of Bilateral Carotid Body Resection on Central CO2 Sensitivity

BackgroundHuman breathing is regulated by feedback and feed-forward control mechanisms, allowing a strict matching between metabolic needs and the uptake of oxygen in the lungs. The most important control mechanism, the metabolic ventilatory control system, is fine-tuned by two sets of chemoreceptors, the peripheral chemoreceptors in the carotid bodies (located in the bifurcation of the common carotid arteries) and the central CO2 chemoreceptors in the ventral medulla. Animal data indicate that resection of the carotid bodies results, apart from the loss of the peripheral chemoreceptors, in reduced activity of the central CO2 sensors. We assessed the acute and chronic effect of carotid body resection in three humans who underwent bilateral carotid body resection (bCBR) after developing carotid body tumors.Methods and FindingsThe three patients (two men, one woman) were suffering from a hereditary form of carotid body tumors. They were studied prior to surgery and at regular intervals for 2–4 y following bCBR. We obtained inspired minute ventilation (Vi) responses to hypoxia and CO2. The Vi-CO2 responses were separated into a peripheral (fast) response and a central (slow) response with a two-compartment model of the ventilatory control system. Following surgery the ventilatory CO2 sensitivity of the peripheral chemoreceptors and the hypoxic responses were not different from zero or below 10% of preoperative values. The ventilatory CO2 sensitivity of the central chemoreceptors decreased by about 75% after surgery, with peak reduction occurring between 3 and 6 mo postoperatively. This was followed by a slow return to values close to preoperative values within 2 y. During this slow return, the Vi-CO2 response shifted slowly to the right by about 8 mm Hg.ConclusionsThe reduction in central Vi-CO2 sensitivity after the loss of the carotid bodies suggests that the carotid bodies exert a tonic drive or tonic facilitation on the output of the central chemoreceptors that is lost upon their resection. The observed return of the central CO2 sensitivity is clear evidence for central plasticity within the ventilatory control system. Our data, although of limited sample size, indicate that the response mechanisms of the ventilatory control system are not static but depend on afferent input and exhibit a large degree of restoration or plasticity. In addition, the permanent absence of the breathing response to hypoxia after bCBR may aggravate the pathological consequences of sleep-disordered breathing.

Modeling the ventilatory response to variations in end-tidal PCO2 in patients who have undergone bilateral carotid body resection.

Studies on patients who have had bilateral carotid body resection for the relief of asthmatic symptoms1,2 or bilateral carotid endarterectomy for transient cerebral ischemia3 suggest that the fast component of ventilatory response to CO2 arises from carotid body activity. However it is also possible that the effect on the ventilatory response to CO2 was related to their underlying respiratory or vascular disease. The current study sought to examine the ventilatory responses to CO2 of adult human subjects who had undergone bilateral carotid body resections for glomus tumors. These subjects have normal lung and vascular function.

A new aspect of the carotid body function controlling hypoxic ventilatory decline in humans.

Ventilatory response to eucapnic sustained mild hypoxia was measured in one patient with unilateral and three patients with bilateral carotid body (CB) resection (defined UR and BR, respectively). The profile of ventilatory response in UR patient was initially augmented then gradually declined (biphasic pattern) as generally seen in normal subjects although the absolute magnitude was substantially low. On the other hand, biphasic pattern was disappeared in all three BRs. Lack of hypoxic ventilatory decline (HVD) in the late period of sustained hypoxia was in marked contrast to that reported in the anaesthetized and CB-denervated animals whose ventilation was severely depressed lower than the pre-hypoxic control level. In view of recent knowledge that the analogous mild hypoxia in normal animals and humans elicits an useful adaptation to economize energy expenditure with maintaining reversible excitability in control of respiration, BR patients were considered to have lost this ability. We conclude that in awake humans the CB not only stimulates ventilation but also controls the degree of subsequent HVD during sustained hypoxia.

Physiologic Changes following Bilateral Carotid-Body Resection in Patients with Chronic Obstructive Pulmonary Disease

In an attempt to establish the characteristic pattern of change in (1) indices of pulmonary function, (2) arterial blood gas, and (3) arterial acid-base status which result from bilateral carotid body resection (BCBR), we analyzed the results of 146 consecutive patients with severe chronic obstructive pulmonary disease who had undergone BCBR at a single hospital site. In addition, we analyzed the results of incremental exercise testing in 21 similar patients, performed at a separate hospital. On average, TLC, FRC, and RV all decreased after surgery, whereas FEV1 increased. Although the data were highly variable, PaO2 decreased on average in proportion to the increase in PaCO2. The smaller group exercised to a higher metabolic rate after surgery; maximum ventilation, however, was unchanged. This led to a further fall in PaO2 and increase in PaCO2. We conclude that individual patient responses to BCBR are highly variable, but the procedure typically results in a small further hypoxemia and hypercapnia with no further impairment to pulmonary function.

Bilateral Carotid Body Resection for the Relief of Dyspnea in Severe Chronic Obstructive Pulmonary Disease: Physiologic and Clinical Observations in Three Patients

For many patients with advanced chronic airflow limitation (COPD) the treatment of dyspnea remains inadequate despite medications, rehabilitation programs, and supplemental oxygen. Bilateral carotid body resection (BCBR) is a controversial operation which has been reported anecdotally to relieve dyspnea in such patients, but its risks and long-term effects are not known. We studied pulmonary function and the ventilatory response to exercise of three severely dyspneic COPD patients who had chosen independently and without our knowledge to undergo this operation. All three patients reported improvement in dyspnea following BCBR despite the absence of improvement in their severe airflow limitation (mean FEV1 = 0.71 L before and 0.67 L after BCBR). The three patients died 6, 18 and 36 months after the removal of their carotid bodies, still convinced of the efficacy of their surgery. Their reported relief of dyspnea was associated with substantial decreases in minute ventilation and deterioration in arterial blood gases. Arterial blood gases worsened both at rest (PO2 fell from 57 to 45 mm Hg; PCO2 rose from 45 to 57 mm Hg) and during identical steady state exercise (at peak exercise, PO2 fell from 46 to 37 mm Hg and PCO2 rose from 50 to 61 mm Hg) postoperatively. Total minute ventilation decreased postoperatively both at rest (-3.4 L/min, -25 percent) and with exercise (-9.4 L/min, -39 percent) primarily because of decreases in respiratory rate (from 21 to 16 breaths/min at rest and from 25 to 18 breaths/min with exercise), and this was associated with decreases in both oxygen uptake (-26 percent) and carbon dioxide production (-22 percent) for the same external exercise workload. Whether the reported improvement in dyspnea was due to decrease in ventilation resulting from decrease in respiratory drive, a surgical placebo effect or some other unestablished effect of removal of the carotid bodies deserves further study.

Bilateral carotid body resection in man enhances hypoxic tachycardia.

In three groups of subjects we studied heart rate (HR) and ventilatory responses to progressive eucapnic hypoxia, steady-state hypercapnia with and without hypoxia, and hyperoxic and hypoxic breathholding (BH). Groups were six subjects about 25 years after bilateral carotid body resection (BR), eight subjects of an equally long period after unilateral resection (UR), and three control subjects similar to the study groups in age and pulmonary function (C). During progressive hypoxia, HR increased more in BR than in UR and C subjects. Ventilatory response was lowest in BR subjects (as expected). Steady-state hypoxic hypercapnia (end-tidal PO2, 60 Torr) depressed HR significantly more in C than in BR and UR subjects. Again, ventilatory response was lower in BR than in C subjects. HR progressively increased during BH initiated in hyperoxia (end-tidal PO2, 200 Torr) and hypoxia (end-tidal PO2, 70 Torr). In the BR group, the HR increment during hypoxia was significantly larger than that during hyperoxia. No such difference was apparent in UR and C groups. Thus, hypoxia with or without hypercapnia tends to accelerate HR in BR subjects whereas either less tachycardia or slowing is seen in UR and C subjects.

Role of carotid chemoreceptors in control of breathing at rest and in exercise: Studies on human subjects with bilateral carotid body resection.

Control of ventilation at rest and in exercise was studied in subjects whose carotid bodies were bilaterally resected (BR) for the treatment of bronchial asthma some 30 years ago. Ventilatory activities of the carotid body were estimated to be responsible for about 90% and about 30% of the hypoxic and hypercapnic responses, respectively. The BR subjects still revealed a weak hypoxic chemosensitivity, called residual hypoxic response (RHR). The nature of RHR was discussed in detail. Exercise hyperpnea was found to be depressed in the BR subjects when compared with the subjects with similarly impared pulmonary function. This result appears to support the oscillation hypothesis in explaining exercise hyperpnea.

Bilateral Carotid Body Resection in Children with Severe Bronchial Asthma: A Retrospective Study

Bilateral Carotid Body Resection in Children with Severe Bronchial Asthma: A Retrospective Study

Decreased exercise hyperpnea in patients with bilateral carotid chemoreceptor resection.

Exercise hyperpnea was compared in 5 asthmatics 25 yr after bilateral carotid body resection (BR), 4 others 19 yr after unilateral resection (UR), and 12 controls (C) matched for age and pulmonary flow limitation. In the BR group, ventilation rose less with exercise, mostly because BR experienced less tachypnea. End-tidal PCO2 rose 5.8 +/- 3.2 (P less than 0.05) to 46 Torr at 50 W. In UR and C the same load did not increase PETCO2 significantly (+2.1 and +1.4 Torr, respectively). Arterial-end-tidal PCO2 differences before and 15--45 s postexercise were insignificant in all three groups. Heart rate and blood pressure rose equally in the three groups, suggesting that the ventilatory effects were not secondary to blood flow differences and disclosing no evidence of baroreceptor denervation during glomectomy.

Impaired response to hypoxia after bilateral carotid body resection for treatment of bronchial asthma: K. C. Chang, C. G. Morrill, and H. Chai. Chest 73:667–669 (May), 1978

Impaired response to hypoxia after bilateral carotid body resection for treatment of bronchial asthma: K. C. Chang, C. G. Morrill, and H. Chai. Chest 73:667–669 (May), 1978

Impaired Response to Hypoxia after Bilateral Carotid Body Resection for Treatment of Bronchial Asthma

Decreased ventilatory responsiveness to isocapnic hypoxia and increased breath-holding times were measured in a 12-year-old asthmatic boy who had undergone bilateral resection of the carotid bodies. The patient had episodes of cyanosis in which he became disoriented, but he had no subjective feelings of discomfort or dyspnea.

Mechanism of respiratory responses to intravenous NaHCO3, HCl, and KCN

We studied the mechanism by which respiratory responses are produced by rapid injection of NaHCO3, HCl, or KCN into the superior vena cava of lightly anesthetized dogs. To estimate independently circulatory transit time to receptor sites, the solutions were injected at 0 degrees C and their arrival time at the ascending aorta and carotid sinus was detected by thermocouples. All of the ventilatory responses were observed to begin after the substances had reached the ascending aorta and 94% began after the carotid sinus had been reached. The injections were repeated following bilateral vagotomy and/or carotid body resection. Vagotomy produced no significant changes in ventilatory responses, but carotid body resection considerably reduced them. Following both procedures, few ventilatory responses were observed, and the time lag to the onset of the response increased greatly. We conclude that all of the observed ventilatory responses can be accounted for by the known arterial and central chemoreceptors, and that no evidence for pulmonary chemoreceptors was obtained.

Erythropoiesis in Carotid Body Resected Cats

Abstract It has been reported that removal of carotid bodies in cats results in a brief, profuse reticulocytosis followed by depression to below-normal levels of reticulocytes and a progressively severe anemia. Injection of cat carotid body extract was reported to increase erythrocyte 59Fe incorporation in polycythemic rats. Other studies could find no hematological abnormality in humans after bilateral carotid body resection. We reexamined the effect of carotid body resection in the cat with serial bone marrow aspirations, hematocrit determination, and reticulocyte determination. T1/2 for plasma 59Fe removal, erythrocyte 59Fe incorporation, and 51Cr lifespan determinations were performed on five operated and three control cats. No significant differences were found. We conclude that the carotid body has no direct effect on erythropoiesis and that the anemia reported in a prior study was secondary to sepsis resulting from an indwelling femoral vein catheter.

A Role for the Carotid Body in Cardiovascular Control in Man

The carotid bodies play a role in the pressor response to hypoxemia in experimental animals. To determine the importance of the carotid bodies in cardiovascular control in man, we investigated eight subjects who had had (at other institutions) bilateral carotid body resection (CBR), without baroreceptor denervation, for bronchial asthma. Five normal subjects and three asthmatic patients served as controls. The subjects breathed air, 12 percent O₂ in N₂, and 5 percent CO₂, 21 percent O₂ in N₂ at rest and during cycle ergometer exercise. During hypoxia (PaO₂ = 40 mm Hg), the tachycardia was not affected by CBR; the heart rate increase averaged 15 beats per minute during rest and exercise. The systolic, diastolic and pulse pressures slowly decreased in the CBR subjects (avg systolic ↓ = 14 mm Hg), whereas it increased in the control subjects (avg systolic ↑ = 12 mm Hg). Following return to air breathing, blood pressure decreased in the control, whereas it increased in the CBR subjects. In contrast to the altered response of blood pressure in CBR subjects during hypoxia, the pressor response to hypercapnia was not different in the two groups. We conclude that in man, the carotid bodies are essential for normal pressor responses during hypoxia, but not for the tachycardia of hypoxia or the cardiovascular responses to hypercapnia.