Adult carotid chemoafferent responses to hypoxia after 1, 2, and 4 wk of  postnatal hyperoxia

Bisgard, G. E.; Olson, E. B.; Wang, Z.-Y.; Bavis, Ryan W.; Fuller, David D.; Mitchell, Gordon S.

doi:10.1152/japplphysiol.00985.2002

Cited by 76 publications

(56 citation statements)

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“…Some of these soma are most likely from chemoafferent cells. Increased tissue levels of ROS within chemoafferent cell bodies may account for histologic evidence of cytotoxicity and ablation of hypoxic chemosensitivity in these cells, in newborn rats exposed to hyperoxia (10).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Hyperoxia on Reactive Oxygen Species (ROS) in Rat Petrosal Ganglion Neurons During Development Using Organotypic Slices

Kwak

Gauda

2006

Pediatr Res

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Hyperoxia, during development in rats, results in hypoxic chemosensitivity ablation, carotid body hypoplasia, and reduced chemoafferents. We hypothesized that hyperoxia increases reactive oxygen species (ROS) in cell bodies of chemoafferents. Organotypic slices of petrosal-nodose ganglia from rats at day of life (DOL) 5-6 and 17-18 were exposed to 8%, 21%, or 95% O 2 for 4 h in the presence or absence of the ROS-sensitive fluorescent indicator, CM-H 2 DCFDA, and propidium iodide was used to determine the relationship between cell death and oxygen tension. In tissue slices from DOL 5-6 rats, fluorescence intensity was 182.5 Ϯ 2.9 for hypoxia, 217.5 Ϯ 3.3 for normoxia, and 336.6 Ϯ 3.8 for hyperoxia, (mean Ϯ SEM, p Ͻ 0.001, ANOVA). Normoxia increased ROS levels by 19.2% from hypoxia (p Ͻ 0.01) with a further increase of 54.8% from normoxia to hyperoxia (p Ͻ 0.001). In tissue slices from DOL 17-18 rats, ROS levels increased with increasing oxygen tension but were less than in younger animals (p Ͻ 0.01, ANOVA). The antioxidants, NAC and TEMPO-9-AC, attenuated ROS levels and cell death. Electron microscopy demonstrated that hyperoxia damages the ultrastructure within petrosal ganglion neurons. Hyperoxic-induced increased levels of ROS in petrosal ganglion neurons may contribute to loss of hypoxic chemosensitivity during early postnatal development. N umerous studies in mammalian species support a role for peripheral arterial chemoreceptors in stabilizing ventilation at a critical period during early postnatal development, which establishes rhythmogenesis that is sustained throughout life (1,2). The components of the peripheral arterial chemoreceptors are found within the carotid body that is located in the bifurcation of the carotid artery and consists of three major neuronal components that include: 1) type I chemosensory cells, also known as glomus cells, which contain neurotransmitters and autoreceptors; 2) type II cells, which are similar to supportive glial cells; and 3) chemoafferent nerve fibers from the carotid sinus nerve, a branch of the IX cranial nerve, with cell bodies in the petrosal ganglion (PG) (3,4).Exposure to chronic hyperoxia, during the first weeks of postnatal development, depresses ventilatory responses to subsequent acute hypoxia in newborn animals and in premature infants (5-7). Hyperoxic exposure in newborn rat pups is cytotoxic to peripheral arterial chemoreceptors as evidenced by hypoplasia of the carotid body and a 41% reduction in the number of chemoafferent neurons (8). The mechanisms leading to cytotoxic changes in the carotid body and the reduction in chemoreflexes after hyperoxicexposure during early postnatal development are unknown. In other model systems, hyperoxia is associated with increased production of ROS, including superoxide, hydroxyl radical, and hydrogen peroxide, which can contribute to cellular damage via lipid peroxidation, enzyme inactivation, and protein and nucleic acid oxidation, resulting in apoptosis or necrosis (9). Using a novel ex vivo organotypic s...

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Section: Discussionmentioning

confidence: 99%

The Effect of Hyperoxia on Reactive Oxygen Species (ROS) in Rat Petrosal Ganglion Neurons During Development Using Organotypic Slices

Kwak

Gauda

2006

Pediatr Res

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“…Thus the presence of normoxia during the first 7-10 days of postnatal life in rats is critical for development of chemoreceptor sensitivity (1,2,7,15,29). Hypoxia causes injury to the developing brain (22,34,57) and could target structures involved in cardiovascular reflexes (4,13,32,49).…”

mentioning

confidence: 99%

Postnatal intermittent hypoxia alters baroreflex function in adult rats

Soukhova-O'Hare

Cheng

Roberts

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Soukhova-O'Hare, Galia K., Zixi (Jack) Cheng, Andrew M. Roberts, and David Gozal. Postnatal intermittent hypoxia alters baroreflex function in adult rats. Am J Physiol Heart Circ Physiol 290: H1157-H1164, 2006. First published September 9, 2005 doi:10.1152/ajpheart.00767.2005.-Chronic perinatal intermittent hypoxia (IH) could have long-term cardiovascular effects by altering baroreflex function. To examine this hypothesis, we exposed rats (n ϭ 6/group) for postnatal days 1-30 or prenatal embryonic days 5-21 to IH (8% ambient O2 for 90 s after 90 s of 21% of O2, 12 h/day) or to normoxia (control). Baroreflex sensitivity (BRS) and cardiac chronotropic responses were examined in anesthetized animals 3.5-5 mo later by infusing phenylephrine or sodium nitroprusside (6 -12 g/min iv, 1-2 min) during normoxia and after 18 min of acute IH (IHA). In controls after IHA, baroreflex gain was 42% (P Ͻ 0.05) less than during normoxia. BRS in the postnatal IH group during normoxia was ϳ50% less than in control rats and similar to controls after IHA. The heart rate response to phenylephrine in the IH group was also less than in controls (P Ͻ 0.05) and was not changed by IHA. BRS and heart rate responses in the prenatal IH group were similar to the normoxic control group. Vagal efferent projections to atrial ganglia neurons in rats after postnatal IH (n ϭ 4) were examined by injecting tracer into the left nucleus ambiguus. After 35 days of postnatal IH, basket ending density was reduced by 17% (P Ͻ 0.001) and vagal axon varicose contacts by 56% (P Ͻ 0.001) compared with controls. We conclude that reduction of vagal efferent projections in cardiac ganglia could be a cause of long-term modifications in baroreflex function.perinatal intermittent hypoxia; vagus; atrial ganglia; basket endings RECURRENT APNEAS THAT CAUSE oxygen desaturation and bradycardia are often present in preterm infants (33). However, the long-term effects of neonatal intermittent hypoxia (IH) on cardiovascular regulation and sympathovagal balance are not well known. Adults who experience IH during sleep-disordered breathing such as obstructive sleep apnea have a high risk of developing hypertension, myocardial ischemia, and heart failure (40, 52). Sympathetic overactivity, decreased baroreflex sensitivity (BRS), and decreased heart rate variability have been found in these patients (6,30,36,37,46). In a rodent model of obstructive sleep apnea, Fletcher et al. (16) demonstrated blood pressure elevation after 30-day exposure to IH. Involvement of the sympathetic efferent arm of the arterial chemoreflex arc was suggested by prevention of the blood pressure response after pharmacological sympathetic blockade or carotid body deafferentiation (16 -19, 50). On the other hand, withdrawal of parasympathetic activity could also contribute to the alteration of sympathovagal balance observed in obstructive sleep apnea, as shown by power spectrum analysis of heart rate variability (26,35,55).Perinatal susceptibility to hypoxia is characterized by the developmental window...

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“…Ling et al showed that the long-term facilitation of ventilatory responses is greater in 1-month-old rats than in 2-month-old rats [76]. And the initial 4 weeks of life are important for the maturation of the carotid body and chemoreflex responses, since previously exposure to hyperoxia throughout the period of 1-4 weeks of age result in an attenuation of the ventilatory and phrenic responses to acute hypoxia [77]. Reeves et al demonstrated that exposure to CIH during the first 30 days of life exhibited a decrease in the number of neurons that receiving vagal and glossopharyngeal projections in the NTS and nucleus ambiguus in accompany with an augmentation in the number of neurones receiving projections in the RVLM [78].…”

Section: The Role Of Nts and Rvlm In Cih Conditionmentioning

confidence: 99%

The Nervous Mechanism of Sympathetic over Activity Induced by Chronic Intermittent Hypoxia

En¹

2014

J Pulm Respir Med

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Hypertension is concerned to be a common complication in Chronic Intermittent Hypoxia (CIH) conditions which mimic the state of Obstructive Sleep Apnoea (OSA) in clinic. Sympathoexcitation is a crucial origin in the process of high blood pressure and the mechanisms involved in the sympathoexicitatory changes after CIH exposure are complex referring to chemoreflex, baroreflex, neurotransmitters, and central nuclei and so on. In this review we predominantly expound the effect of CIH-induced potentiated Carotid Body (CB) chemoreceptor sensitivity to hypoxia stimulation which results in the enhancement of RSNA and Endothelin (ET) is mentioned due to its expression in CB and the fact that ET is thought to be a significant chemoreceptor-excitatory transmitter. Previously studies have shown expression of ET and ET receptors in the CB chemoreceptor glomus cells and vessel system, and CIH obviously increased the expression which indicated a possible effect of ET to the potentiated ventilatory and cardiovascular responses to acute hypoxia probably via increased inward Ca 2+ currents, inflammatory response or Acid-Sensitive Ion Channels (ASICs) in chemoafferent neurons in the petrosal ganglion. However we also display the effect of enhanced central respiratory-sympathetic coupling which also participated in the increase in sympathetic activity. The other mechanism introduced in this review is the role of the Nucleus Tractus Solitarius (NTS) after CIH exposure. Neurotransmitters like ET and Glutamate act on the cerebroventricle and the NTS elicit significantly increase of RSNA in CIH group. The sympathetic nerve originated site Rostral Ventrolateral Medulla (RVLM) also makes adaptive changes after CIH to copes the hypoxia stimulation and induces RSNA responses. At last we raise the phenomenon that depressed baroreflex sensitivity emerged after a long time CIH exposure and is involved in the process of sustained high blood pressure.

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Adult carotid chemoafferent responses to hypoxia after 1, 2, and 4 wk of postnatal hyperoxia

Cited by 76 publications

References 16 publications

The Effect of Hyperoxia on Reactive Oxygen Species (ROS) in Rat Petrosal Ganglion Neurons During Development Using Organotypic Slices

The Effect of Hyperoxia on Reactive Oxygen Species (ROS) in Rat Petrosal Ganglion Neurons During Development Using Organotypic Slices

Postnatal intermittent hypoxia alters baroreflex function in adult rats

The Nervous Mechanism of Sympathetic over Activity Induced by Chronic Intermittent Hypoxia

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