Carotid Sinus Nerve Research Articles

Commentary: Oxygen regulation of breathing through an olfactory receptor activated by lactate.

Commentary: Oxygen regulation of breathing through an olfactory receptor activated by lactate.

Adrenaline release evokes hyperpnoea and an increase in ventilatory CO2 sensitivity during hypoglycaemia: a role for the carotid body

Hypoglycaemia is counteracted by release of hormones and an increase in ventilation and CO2 sensitivity to restore blood glucose levels and prevent a fall in blood pH. The full counter-regulatory response and an appropriate increase in ventilation is dependent on carotid body stimulation. We show that the hypoglycaemia-induced increase in ventilation and CO2 sensitivity is abolished by preventing adrenaline release or blocking its receptors. Physiological levels of adrenaline mimicked the effect of hypoglycaemia on ventilation and CO2 sensitivity. These results suggest that adrenaline, rather than low glucose, is an adequate stimulus for the carotid body-mediated changes in ventilation and CO2 sensitivity during hypoglycaemia to prevent a serious acidosis in poorly controlled diabetes. Hypoglycaemia in vivo induces a counter-regulatory response that involves the release of hormones to restore blood glucose levels. Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea that maintains arterial CO2 levels and prevents respiratory acidosis in the face of increased metabolism. It is unclear whether the carotid body is directly stimulated by low glucose or by a counter-regulatory hormone such as adrenaline. Minute ventilation was recorded during infusion of insulin-induced hypoglycaemia (8-17mIUkg(-1) min(-1) ) in Alfaxan-anaesthetised male Wistar rats. Hypoglycaemia significantly augmented minute ventilation (123±4 to 143±7mlmin(-1) ) and CO2 sensitivity (3.3±0.3 to 4.4±0.4mlmin(-1) mmHg(-1) ). These effects were abolished by either β-adrenoreceptor blockade with propranolol or adrenalectomy. In this hypermetabolic, hypoglycaemic state, propranolol stimulated a rise in P aC O2, suggestive of a ventilation-metabolism mismatch. Infusion of adrenaline (1μgkg(-1) min(-1) ) increased minute ventilation (145±4 to 173±5mlmin(-1) ) without altering P aC O2 or pH and enhanced ventilatory CO2 sensitivity (3.4±0.4 to 5.1±0.8mlmin(-1) mmHg(-1) ). These effects were attenuated by either resection of the carotid sinus nerve or propranolol. Physiological concentrations of adrenaline increased the CO2 sensitivity of freshly dissociated carotid body type I cells in vitro. These findings suggest that adrenaline release can account for the ventilatory hyperpnoea observed during hypoglycaemia by an augmented carotid body and whole body ventilatory CO2 sensitivity.

Developmental Window Exists in the Hypoxic Ventilatory Response of Juvenile and Adult Male Rats Following Carotid Sinus Nerve Transection

The carotid bodies (CB) are peripheral chemoreceptors that respond to hypoxia by stimulating breathing and increasing blood pressure in order to restore oxygen (O2) levels. The carotid body activates chemosensory afferent terminals of the carotid sinus nerve (CSN), which stimulate the brainstem to increase ventilation. Data from our lab suggests a critical developmental window exists in which the hypoxic ventilatory response (HVR) switches from neonatal to adult. This hypoxic ventilatory response (HVR) seen in male adult rats is blunted after bilateral carotid sinus nerve transection (CSNX). Our objective is to determine the HVR of juvenile male Sprague Dawley rats before and after bilateral CSNX. To test this we performed CSNX at postnatal (P) age P21, and exposed the rats to hypoxia (10% O2) using the BUXCO unstrained, awake, whole‐body plethysmography system four days post surgery. Our results suggest the HVR seen in control juvenile rats is blunted compared to adult rats (n= 12 juvenile and n = 9 adult). Also, after CSNX the juvenile rats exhibit a more diminished HVR compared to adult rats (n = 3 juvenile and n = 9 adult). This data suggests that in control male rats, a critical developmental window may exist in which the carotid body becomes fully sensitized to low blood O2, thus allowing the greater HVR seen in the adult. In addition, our data shows that a secondary means of responding to hypoxia after CSNX may not have functionally developed in the juvenile rats.Support or Funding InformationNIH PO1‐HL1018710

Hypoventilation in the Mdx Mouse Model of Duchenne Muscular Dystrophy

Duchenne muscular dystrophy (DMD) is a fatal genetic disease caused by a lack of the structural protein dystrophin. Patients have severe muscle wasting and chronic respiratory insufficiency. Hypoventilation and sleep disordered breathing are both common features of the disease and are known to culminate in periods of hypoxaemia and hypercapnia. There is a paucity of information regarding the control of breathing in animal models of DMD. We measured ventilation, oxygen consumption (VO2) and carbon dioxide (VCO2) production in freely behaving mdx (dystrophin deficient; n=11) and wild‐type (WT; n=10) mice at 8 weeks of age. qRT‐PCR was used to examine inflammation and hypoxia associated gene expression in diaphragm muscle from WT and mdx mice. Minute ventilation (VE; whole‐body plethysmography) was significantly reduced in mdx mice compared with WT controls (30% reduction). There was no significant difference in VO2 and VCO2 when expressed in absolute terms. Carotid sinus nerve unitary discharge was significantly depressed during normoxia in mdx (n=6) compared with WT (n=6) ex vivo perfused preparations. NF‐kB and TNF‐α mRNA expression were both significantly increased in mdx diaphragm compared with WT. HIF‐1α was significantly increased, while HIF‐2α was significantly decreased in mdx diaphragm muscle. Young mdx mice hypoventilate during air breathing (decreased VE/VCO2), which likely relates to reduced carotid body discharge during normoxia. Mdx diaphragm muscle is in a pro‐inflammatory state and there is differential expression of hypoxia associated genes. We reveal that respiratory control is altered in the mdx mouse model of DMD at a young age.Support or Funding InformationFunded by the Department of Physiology, School of Medicine, University College Cork and Muscular Dystrophy Ireland.

Electrical Stimulation of the Carotid Sinus Nerve Improves Hemodynamics and Heart Rate Variability in L‐NAME Hypertensive Rats

Baroreflex activation by electrical stimulation of the carotid sinus (CS) has been recently used to treat resistant hypertensive patients. In the present study, we evaluated the effects of long‐term electrical stimulation (ES) of CS in L‐NAME hypertensive rats.Hypertension was induced in male Wistar rats by administration of L‐NAME (70 mg/kg, per os) for 10 days. 7 days after initiating L‐NAME administration the animals were anesthetized and implanted with a catheter into the femoral artery and received, subcutaneously, a miniaturized battery‐operated electrical stimulator connected to electrodes placed around the left CS. On the following day, basal AP was directly recorded for 60 min and the stimulator was turned on. Electrical pulses (1 ms, 3 V, 30 Hz) were delivered to the CS, intermittently (20/20s ‐ on/off), for the next 48 h. Basal mean arterial pressure (AP) from L‐NAME hypertensive rats was 176±3 mmHg but showed a marked fall (D= −51±5 mmHg) at the onset of ES of the CS. At the end of the stimulation period only a mild rise in AP was seen; however, the AP recorded during the first 60 min after ES of the CS was lower (159±3 mmHg) than before the stimulation period. Spectral analysis showed that ES of the CS reduced the LF power of AP spectra (10.0±1.9 to 3.7±0.4 mmHg2, p=0.014) and also increased the power of PI spectra at HF range (1.8±0.4 to 3.4±0.8 ms2, p=0.028). Moreover, LF/HF ratio of PI spectra was also markedly reduced after the stimulation period (0.42±0.09 to 0.14±0.02, p<0.01). In conclusion, ES of the CS for 48 h was effective to reduce the AP lasting 1 h after the stimulation period. In addition, the AP and heart rate variability strongly suggests a lower sympathetic modulation upon the cardiovascular system after ES of the CS in L‐NAME hypertensive rats.Support or Funding InformationFAPESP, CAPES, CNPq, FAEPA

Оценка влияния синус-сберегающих модификаций каротидной эндартерэктомии на вегетативную регуляцию и центральную гемодинамику

BackgroundSuch complications as myocardial infarction, hyperperfusion syndrome and its effects, postoperative hematomes constitute a life-threatening event during early follow-up of carotid surgery. One of the main risk factors for these complications is a variation of central hemodynamics, especially that leading to arterial hypertension.ObjectiveThe study aimed to evaluate the safety of carotid sinus surgery as a way of preventing arterial hypertension after carotid artery reconstructions. The other objective was to compare the resultant data with the heart rate variations obtained during rhythmocardiography.MethodsThe study focused on central hemodynamics indicators and included 290 cases. All patients were broken down in two groups. 167 patients of the first group underwent dissection of carotid sinus nerves. The carotid sinus nerves of patients from the second group (123 patients) were kept intact. Analysis of autonomic regulation of 13 patients from the first group and 17 patients from the other one was then carried out, with the heart rate variations accurately estimated at the neurocardiological laboratory.ResultsOn the first postoperative day all hemodynamic indicators (such as SBP, DBP, pulse pressure, heart rate) in the second group were lower than those in the first group of patients (p<0.05), while tending to recover by the third day. This fact kept postoperative complications to a minimum. The patients from the second group also demonstrated a lower activity of the sympathetic nervous system and a higher activity of the parasympathetic one. These results explain the difference between the central hemodynamic indicators in two groups.ConclusionCarotid sinus-saving surgery decreases the risk of early postoperative complications caused by arterial hypertension.

The Use of Neuronavigation with Vasular Microdoppler in Transsphenoidal Pituitary Surgery

Object: To evaluate the use of neuronavigation with vascular micro-doppler in transsphenoidal pituitary surgery. Methods: 141 cases having done transsphenoidal pituitary surgery are evaluated from 2005 to 2014. Fluoroscopy was used in 69 cases and vascular micro-doppler with neuronavigation were used in 72 cases. Results: Transsphenoidal surgery has a lot of risks due to sella’s deep location, and position of the carotid artery and the optic nerve. Clasically the fluoroscopy and microscopic anatomical markers were used in order to minimize the risk of carotid artery and optic nerve damage. Additional devices such as neuronavigation and vascular micro-doppler are needed to decrease the morbidity and mortality arising from these injuries. Conclusion: Neurovascular complications such as carotid artery and optic nerve injuries owing to disorientation in transsphenoidal surgery will reduce the use of neuronavigation with vascular micro-doppler.

Identification and Characterization of GAL-021 as a Novel Breathing Control Modulator.

The authors describe the preclinical pharmacological properties of GAL-021, a novel peripheral chemoreceptor modulator. The ventilatory effects of GAL-021 were characterized using tracheal pneumotachometry (n = 4 to 6), plethysmography (n = 5 to 6), arterial blood gas analyses (n = 6 to 11), and nasal capnography (n = 3 to 4) in naive animals and those subjected to morphine-induced respiratory depression. Morphine analgesia in rats was evaluated by tail-flick test (n = 6). Carotid body involvement in GAL-021 ventilatory effects was assessed by comparing responses in intact and carotid sinus nerve-transected rats. Hemodynamic effects of GAL-021 were evaluated in urethane-anesthetized rats (n = 7). The pharmacological profile of GAL-021 in vitro was investigated using radioligand binding, enzyme inhibition, and cellular electrophysiology assays. GAL-021 given intravenously stimulated ventilation and/or attenuated opiate-induced respiratory depression in rats, mice, and nonhuman primates, without decreasing morphine analgesia in rats. GAL-021 did not alter mean arterial pressure but produced a modest increase in heart rate. Ventilatory stimulation in rats was attenuated by carotid sinus nerve transection. GAL-021 inhibited KCa1.1 in GH3 cells, and the evoked ventilatory stimulation was attenuated in Slo1 mice lacking the pore-forming α-subunit of the KCa1.1 channel. GAL-021 behaved as a breathing control modulator in rodents and nonhuman primates and diminished opioid-induced respiratory depression without compromising opioid analgesia. It acted predominantly at the carotid body, in part by inhibiting KCa1.1 channels. Its preclinical profile qualified the compound to enter clinical trials to assess effects on breathing control disorders such as drug (opioid)-induced respiratory depression and sleep apnea.

Oxygen regulation of breathing through an olfactory receptor activated by lactate.

SummaryAnimals have evolved homeostatic responses to changes in oxygen availability that act on different time scales. Although the hypoxia-inducible factor (HIF) transcriptional pathway that controls long term responses to low oxygen (hypoxia) has been established1, the pathway that mediates acute responses to hypoxia in mammals is not well understood. Here we show that the olfactory receptor 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 declines2. 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 hyperventilation3–6, 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.

Subaxial cervical pedicle screw fixation through paraspinal approach: anatomic and clinical studies

Objective To investigate the feasibility and clinical application of the cervical pedicle screw fixation through intermuscular planes between musculus semispinalis cervicis and musculus semispinalis capitis. Methods Five adult specimens were selected for studying the anatomic features of musculus semispinalis cervicis and musculus semispinalis capitis and the distributions of surrounding deep cervical vassels and carotid nerve. Fifty cervical pedicle screws were placed into C3-C7 for all specimens. Besides, cervical transpedicular fixation with 49 screws was performed in 12 patients via the intermuscular planes between musculus semispinalis cervicis and musculus semispinalis capitis. Wounds and complications were detected after operation. Screw position was assessed by CT imaging. Results Musculus semispinalis capitis was the main part of the lateral intermuscular septum. Musculus semispinalis cervicis was the main part of the medial intermuscular septum. Multifidus and rotator participated in forming the cervical dorsal rami nerve bone fiber tube. Medial and lateral intermuscular tissues were dominated respectively by cervical dorsal medial branch and lateral branch. Deep cervical artery lied in upward branches between the semispinalis capitis and semispinalis cervicis, supplying both sides of the semispinalis. Six screws placed in the specimens cut through the pedicle wall. Screws were placed successfully in all the 12 patients. The plane between musculus semispinalis capitis and semispinalis cervicis could be separated easily. Four screws broke the pedicle wall, but there were no screw-related complications. Conclusions A new intermuscular plane through musculus semispinalis cervicis and musculus semispinalis capitis is developed to facilitate the low cervical pedicle screw insertion. Primary clinical results show cervical pedicle screw placement through the new approach is safe, feasible, easy and minimally invasive. Key words: Cervical vertebrae; Anatomy; Pedicle screws

Role of Chemoreceptor Activation in Hemodynamic Responses to Electrical Stimulation of the Carotid Sinus in Conscious Rats.

Electric carotid baroreflex activation has been used to treat patients with resistant hypertension. It is hypothesized that, in conscious rats, combined activation of carotid baro- and chemoreceptors afferences attenuates the reflex hypotension. Rats were divided into 4 groups: (1) control group, with unilateral denervation of the right carotid chemoreceptors; (2) chemoreceptor denervation group, with bilateral ligation of the carotid body artery; (3) baroreceptor denervation group, with unilateral denervation of the left carotid baroreceptors and right carotid chemoreceptors; and (4) carotid bifurcation denervation group, with denervation of the left carotid baroreceptors and chemoreceptors, plus denervation of the right carotid chemoreceptors. Animals were subjected to 4 rounds of electric stimulation (5 V, 1 ms), with 15, 30, 60, and 90 Hz applied randomly for 20 s. Electric stimulation caused greater hypotensive responses in the chemoreceptor denervation group than in the control group, at 60 Hz (-37 versus -19 mm Hg) and 90 Hz (-33 versus -19 mm Hg). The baroreceptor denervation group showed hypertensive responses at all frequencies of stimulation. In contrast, the carotid sinus denervation group showed no hemodynamic responses. The control group presented no changes in heart rate, whereas the chemoreceptor denervation group and the baroreceptor denervation group showed bradycardic responses. These data demonstrate that carotid chemoreceptor activation attenuates the reflex hypotension caused by combined electric stimulation of the carotid sinus and the carotid sinus nerve in conscious rats. These findings may provide useful insight for clinical studies using baroreflex activation therapy in resistant hypertension and heart failure.

Detailed Anatomy of the Cranial Cervical Ganglion in the Dromedary Camel (Camelus dromedarius).

The detailed morphology and topography of the cranial cervical ganglion (CCG) with its surrounding structures were studied in 10 sides of five heads of adult one-humped camel to determine its general arrangement as well as its differences and similarities to other animals. The following detailed descriptions were obtained: (1) the bilateral CCG was constantly present caudal to cranial base at the rostroventral border of the occipital condyle over the caudolateral part of nasopharynx; (2) the CCG was always in close relations medially with the longus capitis muscle, rostrolaterally with the internal carotid artery, and caudally with the vagus nerve; and (3) the branches of the CCG were the internal carotid and external carotid nerves, jugular nerve, cervical interganglionic branch, laryngopharyngeal branch, carotid sinus branch and communicating branches to the vagus, and first spinal nerves. In conclusion, there was no variation regarding topography of dromedary CCG among the specimens, in spite of typical variations in number, and mainly in origin of nerve branches ramifying from the CCG. In comparative anatomy aspect, the close constant relations, and presence of major nerves (internal/external carotid and jugular nerves) of dromedary CCG exhibited a typical reported animal's pattern. However, the shape, structures lateral to the CCG, the origin and course pattern of external carotid and jugular nerves, the number of the major nerves branches, the communicating branches of the CCG to the spinal and cranial nerves, and the separation of most rostral parts of vagosympathetic trunk of dromedary were different from those of most reported animals.

Microchannel Electrode Stimulation of Deep Peroneal Nerve Fascicles Induced Mean Arterial Depressor Response in Hypertensive Rats

Hypertension (HTN) affects over 1 billion people in the world, and while most are treated effectively with pharmacological regimens, 10–30% of them do not show a beneficial response. Electrical stimulation of the renal sympathetic, vagus and carotid sinus nerves has shown depressor effects and has been proposed as an alternative treatment for resistant hypertension (R-HTN). However, these nerves are heterogeneous in afferent/efferent composition, and their stimulation often results in unwanted side effects. We evaluated the possibility of eliciting a depressor response from stimulation of single fascicle of the somatic deep peroneal nerve (fDPN). A microchannel electrode array (µCEA) was used to stimulate the fDPN at low frequency, which induced a significant (p ≤ 0.03) transient reduction in mean arterial pressure (MAP) with no significant effects on heart rate. The depressor response was prolonged for several hours by extending the fDPN stimulation to 5 min, which induced significant reduction (17–25%) in MAP for up to 4 h. Immunofluorescence evaluation of the axonal marker, myelin, and active macrophages in the fDPN revealed no indication of nerve damage or overt inflammation in response to the procedure. This study provides evidence supporting the use of µCEA interfacing of small somatic nerve fascicles associated with cardiovascular relevant acupoints to induce significant reductions in MAP and opens the possibility of neuromodulation of small fascicles as an alternative strategy to treat R-HTN with minimal side effects. Further, the µCEA multielectrode array offers an effective tool for neuromodulation of small nerve fascicles, enabling a number of possible future medical bioelectronic applications.

Does the Technique of Carotid Endarterectomy Determine Postoperative Hypertension?

Hypertension (HT) after carotid endarterectomy (CEA) is a risk factor for postoperative myocardial infarction, stroke, and neck hematoma. We compared the incidence of postoperative HT within the week after eversion CEA (e-CEA) and patch closure CEA (p-CEA). Postoperative HT was defined as a systolic blood pressure (sBP) ≥ 160 mm Hg and/or the need for postoperative vasodilatators. The aim of our study was to determine if the technique of CEA had an effect on postoperative HT. Between January 2010 and June 2011, we prospectively reviewed 560 consecutive endarterectomies (340 p-CEAs and 220 e-CEAs) performed in 443 patients under general anesthesia. All had >70% stenoses, 119 were symptomatic, and 441 asymptomatic. We compared preoperative, peroperative, and postoperative sBP and diastolic blood pressure, carotid sinus nerve block, postoperative intravenous and oral antihypertensive medications, neurologic and cardiac complications, and mortality. The e-CEA group had a higher incidence of women (36.4% vs. 21.8%, P = 0.0002) and HT (85.0% vs. 78.2%, P = 0.04). The e-CEAs had a significantly higher incidence of carotid sinus nerve block (93.6% vs. 15.6%, P < 0.0001). The incidence of postoperative HT was not significantly different between the 2 groups (75.9% in the e-CEA group versus 68.5% in the p-CEA group, P = 0.06). The average postoperative sBP between postoperative hour (H) 2 and H12 was significantly higher in the e-CEA group but <160 mm Hg. The sBP dropped between H2 and H6, and this decrease was greater in the p-CEA group (30% vs. 15% in the e-CEA group). The need for postoperative antihypertensive medication was not different between the 2 groups. One independent risk factor of postoperative HT was identified: history of HT. The rate of postoperative complications was not significantly different between the 2 groups. The e-CEA technique is not a risk factor and does not have an effect on postoperative HT. The postoperative sBP was more stable in this group. Eversion carotid endarterectomy has been considered, in the literature, as a risk factor of postoperative hypertension. We conducted a large prospective and comparative study of the endarterectomy technique by eversion and with conventional patch closure. The primary end point was the blood pressure value and the administration of antihypertensive treatment. Our study shows that postoperative hypertension after carotid endarterectomy is not related to the surgical technique. Changes in blood pressure after carotid endarterectomy by eversion are lower than those observed after conventional endarterectomy with patch closure. This technique prevents the occurrence of possible hypotension occurrence, which can be the cause of perioperative complications.

Initial experience with therapeutic geometric modification of the carotid bulb for true resistant hypertension

The contribution of carotid baroreceptor feedback in preventing or potentially contributing to the essential hypertensive cascade is poorly understood. It is clear the carotid sinus nerve action potentials are triggered by carotid bulb stretch rather than pressure and are only sustained during pulsatile increases in pressure. In addition, the carotid baroreceptor negative feedback is gradually extinguished in hypertension patients (a phenomenon known as "resetting"). We report a case of significant reduction in blood pressure in a patient with true resistant hypertension after change in the carotid bulb pulsatile strain patterns following the implant of an intravascular prosthesis.

P2X3 receptor‐mediated chemoreceptor hypersensitivity in young spontaneous hypertensive rats

Sympathetic overactivity has been related to the pathogenesis of hypertension. Enhanced peripheral chemoreceptor sensitivity has been suggested as a possible mechanism for sympathetic overactivity. We compared both baseline and chemoreflex evoked carotid sinus nerve (CSN) activity, and the electrophysiological properties of petrosal ganglion cells (PGc) innervating the carotid body in in situ preparations of young spontaneously hypertensive (SH) and Wistar rats. Since ATP plays a major role in chemosensory transduction in the carotid body, we also evaluated the contribution of ATP and P2X receptors in PGc and their involvement in sympathetic overactivity observed in SH rats. SH rats (n=22) presented: increased basal and chemoreflex evoked CSN discharge, and the electrical excitability of PGc was elevated relative to Wistar rats (n=25). A significant increase in the depolarizing effects of ATP and α,β‐methylene ATP in SH (n=18) versus Wistar (n=16) PGc was observed. This was consistent with raised single‐cell mRNA expression of ionotropic P2X3 channels (n=12) in SH rats. Moreover, both the increased baseline and chemoreflex evoked sympathetic nerve response in SH rats (n=12) was markedly reduced after perfusion of the PG with AF‐353, a selective antagonist of P2X3 receptors. Our results suggest that ATP and P2X3 receptors play an important role as a novel mechanism for increased carotid body tone and hyper‐chemosensitivy that contributes to the sympathetic overactivity in SH rats.Support: British Heart Foundation and FAPESP

Lipopolysaccharide(LPS) Exposure During The Early Postnatal Period Reduces The Volume of Type II Cells in The Developing Rat Carotid Body

The carotid body (CB) contains type I(chemoreceptive) and II(supportive) cells, nerve fibres, blood vessels and connective tissues. The rat CB matures in the first two weeks of life, and we recently reported in a rat model of inflammation that hypoxic chemosenstivity of the carotid sinus nerve is attenuated in newborn rats exposed to LPS. Thus, we hypothesized that early postnatal exposure to inflammation leads to morphological changes in developing rat CB. At postnatal day 2 (P2) pups where adminstered LPS(100ug/kg) or saline(SAL) intraperitoneally. At P9-10, one week after exposure, CBs were collected, processed and evaluated with Cavalieri's method for 1) changes in CB volumes, and 2) changes in volume components occupied by Type I and II cells by immunohistochemistry with anti-TH and anti-S-100 antibodies, respectively. Sal group had slightly larger CBs (0.017±0.003 mm3, mean±SD) compared to LPS (0.013±0.003 mm3). While the volume of TH+ component was the same between the treatment groups, the volume of S100+ component was 1.5x less in LPS vs SAL animals(LPS 1.6670*10^6 ± 0.3108*10^6 µm3 vs Sal 2.3090*10^6 ± 0.536*10^6 µm3; Mann-Whitney test, p=0.04). In conclusion, LPS exposure during early postnatal period reduces the number of type II cells in the CB. Since type II can differentiate into type I cells, and participate in co-transmission of hypoxic signaling; a decrease pool of type II cells may adversly effect development and function of the CB leading to breathing disorders.

Effect of Chronic Hypoxia on the Carotid Body Glomus Cell Mitochondrial Response to Acute Hypoxia

Carotid body (CB) glomus cells depolarize in response to hypoxia, causing a [Ca2+]i increase through activation of voltage‐dependent Ca2+ channels, resulting in neurotransmitter release and carotid sinus nerve excitation. Glomus cell mitochondria are believed to be the site of O2 sensing. Previous work showed that perinatal chronic hypoxia (12% O2) during CB postnatal maturation severely impairs CB glomus cell oxygen sensitivity. It is unknown whether chronic hypoxia (CH) impairs glomus cell mitochondrial O2 sensing vs. downstream elements in the O2 transduction cascade. We therefore studied the effects of CH on [Ca2+]i and mitochondrial membrane potential (Δψm) in response to acute hypoxia, in CB glomus cells from rats exposed to hypoxia (10% O2) for 9‐14 days, starting at postnatal day 16‐18 (OxyCycler). Results show that 1) chronic hypoxia severely reduced glomus cell oxygen responsiveness to acute hypoxia as reflected by [Ca2+]i in ~80% of glomus cells; 2) chronic hypoxia did not affect the glomus cell response to 20mM KCl (a non‐specific depolarizing stimulus); 3) chronic hypoxia did not affect Δψm; 4) The reduced glomus cell oxygen sensitivity recovered after CH exposed rats were returned to room air. These results suggest that CH reversibly impairs glomus cell [Ca2+]i in response to acute hypoxia by a mechanism downstream of mitochondria. (Supported by Arkansas Biosciences Institute funds)

PP-132 Eversion and Conventional Carotid Endarterectomy Techniques in Terms of a Comparison of Hypertension

Peripheral Interventions: Imaging in Diagnosis (Abstract nos. PP-132 w PP-142) The American Journal of Cardiology MARCH 26e29, 2015 11 IN AND C PP-132 Eversion and Conventional Carotid Endarterectomy Techniques in Terms of a Comparison of Hypertension. Haydar Yasa, Muhammed Akyuz, Barcin Ozcem, Mehmet Bademci, Nihan Karakas, Banu Akdag Lafci, Tayfun Goktogan, Ali Gurbuz. Bati Anadolu Central Hospital; Ege University; Katip Celebi University Ataturk Training And Research Hospital; Near East University Faculty Of Medicine. Background: The role of carotid endarterectomy for the treatment of carotid bifurcation atherosclerosis is now well established. The operative procedures for carotid stenosis, the eversion techniques require an oblique circumferential incision of the internal carotid artery (ICA) at the carotid bulb and transection of the carotid sinus nerve fibers. In this study, the incidence of postoperative hypertension (HTN) after eversion carotid endarterectomy (E-CEA) was compared with conventional carotid endarterectomy (C-CEA) in the shortand mid-term follow-up periods. Methods: Baseline blood pressures were recorded in all patients 1-2 weeks before the CEA. Systolic blood pressure values and diastolic blood pressure values were 1⁄4.078). The number of patients that had continued administeration of antihypertensive agents were, 4 (5.2%) and 3(3.4%) in the E-CEA group and C-CEA group, respectively. Normalization of arterial blood pressure was achieved in the other patients. No significant postoperative neurological, surgical, or cardiac complications developed in any patient in either group. Conclusion: As a result, the researchers suggest that there is no difference between the two groups after E-CEA control of hypertension at the early and middle periods.

Is the Carotid Body a Metabolic Monitor?

The carotid body is a multi-modal sensor and it has been debated if it senses low glucose. We have hypothesized that the carotid body is modified by some metabolic factors other than glucose and contributes to whole body glucose metabolism. This study examined the roles of insulin, leptin and transient receptor potential (TRP) channels on carotid sinus nerve (CSN) chemoreceptor discharge. In agreement with other studies, CSN activity was not modified by low glucose. Insulin did not affect the CSN hypoxic response. Leptin significantly augmented the CSN response to hypoxia and nonspecific Trp channel blockers (SKF96365, 2-APB) reversed the effect of leptin. Gene expression analysis showed high expression of Trpm3, 6, and 7 channels in the carotid body and petrosal ganglion. The results suggest that the adult mouse carotid body does not sense glucose levels directly. The carotid body may contribute to neural control of glucose metabolism via leptin receptor-mediated TRP channel activation.