Carotid chemoreceptors, systemic blood pressure, and chronic episodic hypoxia mimicking sleep apnea

Fletcher, Eugene C.; Leßke, J.; Behm, Robert; Miller, Charles C.; Stauss, Harald M.; Unger, Thomas

doi:10.1152/jappl.1992.72.5.1978

Cited by 388 publications

(367 citation statements)

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“…A much larger difference between groups was found for mean blood pressure, which was higher in n-IH rats compared with controls. This is strikingly similar to the effects of chronic exposure to IH in adults, which also induces hypertension (12). In adults, this depends on the recurrent activation of peripheral chemoreceptors and is prevented by bilateral carotid body denervation during exposure (12,30), and following chemical sympathetic denervation (13).…”

Section: Respiratory and Hemodynamic Variables In Normoxia In Controlsupporting

confidence: 58%

“…This is strikingly similar to the effects of chronic exposure to IH in adults, which also induces hypertension (12). In adults, this depends on the recurrent activation of peripheral chemoreceptors and is prevented by bilateral carotid body denervation during exposure (12,30), and following chemical sympathetic denervation (13). This is accompanied by an enhanced activity of peripheral chemoreceptors (23,48), chronic sympathetic activation (11,29,31,44), blunted baroreflex responses (3,31), and functional changes in the vascular bed (7).…”

Section: Respiratory and Hemodynamic Variables In Normoxia In Controlmentioning

confidence: 59%

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Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Julien

Niane

Kinkead

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Julien CA, Niane L, Kinkead R, Bairam A, Joseph V. Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia. Am J Physiol Regul Integr Comp Physiol 299: R192-R205, 2010. First published April 21, 2010 doi:10.1152/ajpregu.00707.2009.-We tested the hypothesis that exposure to neonatal intermittent hypoxia (n-IH) in rat pups alters central integrative processes following acute and intermittent peripheral chemoreceptor activation in adults. Newborn male rats were exposed to n-IH or normoxia for 10 consecutive days after birth. We then used both awake and anesthetized 3-to 4-mo-old rats to record ventilation, blood pressure, and phrenic and splanchnic nerve activities to assess responses to peripheral chemoreflex activation (acute hypoxic response) and long-term facilitation (LTF, long-term response after intermittent hypoxia). In anesthetized rats, phrenic and splanchnic nerve activities and hypoxic responses were also recorded with or without intact carotid body afferent signal (bilateral chemodenervation) or in response to electrical stimulations of the carotid sinus nerve. In awake rats, n-IH alters the respiratory pattern (higher frequency and lower tidal volume) and increased arterial blood pressure in normoxia, but the ventilatory response to repeated hypoxic cycles was not altered. In anesthetized rats, phrenic nerve responses to repeated hypoxic cycles or carotid sinus nerve stimulation were not altered by n-IH; however, the splanchnic nerve response was suppressed by n-IH compared with control. In control rats, respiratory LTF was apparent in anesthetized but not in awake animals. In n-IH rats, respiratory LTF was not apparent in awake and anesthetized animals. Following intermittent electrical stimulation, however, phrenic LTF was clearly present in n-IH rats, being similar in magnitude to controls. We conclude that, in adult n-IH rats: 1) arterial blood pressure is elevated, 2) peripheral chemoreceptor responses to hypoxia and its central integration are not altered, but splanchnic nerve response is suppressed, 3) LTF is suppressed, and 4) the mechanisms involved in the generation of LTF are still present but are masked most probably as the result of an augmented inhibitory response to hypoxia in the central nervous system. neonatal intermittent hypoxia; long-term facilitation DEVELOPMENT OF THE RESPIRATORY control system is tightly regulated by complex interactions between genetic and environmental factors that contribute to shape the mature phenotypic expression of this neural network (4). Over the past years, several studies have documented that alterations in environmental oxygen levels during development lead to important changes of the respiratory control system (4). A particular importance has been given to intermittent hypoxic exposure (38, 47, 50) because it may be used in laboratory animals to reproduce some of the effects encountered in human newborn suffering from apneas, which remains one of the major cause...

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Section: Respiratory and Hemodynamic Variables In Normoxia In Controlsupporting

confidence: 58%

Section: Respiratory and Hemodynamic Variables In Normoxia In Controlmentioning

confidence: 59%

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Julien

Niane

Kinkead

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Although a matter of debate, the role of OSAS in the pathogenesis of hypertension is strongly suggested [11,27] , involving markers or pathways indicative of systemic inflammation, such as CRP. Furthermore, in animal studies intermittent hypoxia has been shown to produce hypertension [28,29] . Cardiac arrhythmias appear to be a common in OSAS patients; still their true prevalence remains unknown.…”

Section: Is Crp Part Of the Link Between Cvd And Osas?mentioning

confidence: 99%

Obstructive sleep apnea syndrome and cardiovascular disease: The influence of C-reactive protein

Bouloukaki¹,

Mermigkis²,

Kallergis³

et al. 2015

WJEM

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Obstructive sleep apnea syndrome (OSAS) is a common medical condition, associated with atherosclerosis and cardiovascular disease (CVD). The underlying pathophysiologic mechanisms of this association have not been completely understood and may be multifactorial in origin. A number of studies suggest that inflammatory processes have emerged critical in the pathogenesis of CVD in OSAS. A range of circulating inflammatory molecules has been identified and measured, with a view to assess inflammation and predict vascular damage risk, such as plasma cytokines, adhesion molecules, and C-reactive protein (CRP). CRP is a relevant marker worthy of further study, because not only is elevated in patients with OSAS, but also is rapidly becoming a risk factor for cardiac disease. Furthermore, in selected OSAS patients, aggressive treatment of the disorder may lead to retarding or even improvement of CVD progression. However, still there is a debate on the true correlation between CRP and OSAS, as well as the clinical effect of any reduction after OSAS treatment. Further research is required to define those OSAS patients who will have a considerable reduction with treatment, as well as to understand the significance of the interaction between cardiovascular risk factor and CRP reduction in patients with OSAS.

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“…Chronic intermittent hypoxia (CIH) and activation of arterial carotid body chemoreceptors are primarily responsible for driving the increase in sympathetic activity [4,17]. The excessive sympathetic activity and hypertension are sustained and contribute to high morbidity and mortality in afflicted patients [15,19].…”

mentioning

confidence: 99%

“…Nonetheless, CIH increases sympathetic nerve activity and blood pressure in healthy young animals [4,17]. Therefore, absence of disease and risk factors is unlikely to account for the normal function in elite divers.…”

mentioning

confidence: 99%

CIH: from sleep apnea to breath-hold diving

Chapleau

2010

Clin Auton Res

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Recurrent apneas associated with sleep-disordered breathing increase sympathetic nerve activity and arterial blood pressure, and enhance sympathetic and ventilatory responses to acute hypoxia [14,19]. Chronic intermittent hypoxia (CIH) and activation of arterial carotid body chemoreceptors are primarily responsible for driving the increase in sympathetic activity [4,17]. The excessive sympathetic activity and hypertension are sustained and contribute to high morbidity and mortality in afflicted patients [15,19].Certain recreational and vocational activities involve episodes of volitional apnea. One example is underwater breath-hold diving. In this issue of Clinical Autonomic Research, Breskovic and colleagues [1] address the question: Do elite breath-hold divers exhibit exaggerated increases in muscle sympathetic nerve activity (MSNA) and ventilation during exposure to acute hypoxia? Such a finding would raise concern that the CIH imposed by these types of activities may increase cardiovascular risk in otherwise healthy individuals.The investigators measured arterial oxygen saturation, ventilation, MSNA, blood pressure, heart rate and stroke volume in elite divers and healthy control subjects at baseline (while breathing room air) and during progressive isocapnic hypoxia [1]. Resting blood pressure and MSNA were not significantly different in divers versus control subjects. Furthermore, hypoxia-induced increases in ventilation and MSNA were also not different between the groups. While good news for the divers, these negative results raise several important questions.Is the degree of CIH in divers sufficient to induce sustained sympathetic activation?The frequency of apneas in elite breath-hold divers, at least during the diving season, has been reported to approach that seen in patients with sleep apnea [1][2][3]7]. Furthermore, while a single maximum end-inspiratory breath-hold has little effect on arterial oxygenation in control subjects, the longer maximum breath-hold times in elite divers (up to 6 min, world record = *10 min) are associated with marked arterial oxygen desaturation and pronounced increases in MSNA and blood pressure [5,7]. The chemoreceptor reflex is surely activated when elite divers breath-hold. Thus, it appears likely that the frequency of apneas and degree of hypoxemia were sufficient to induce sympathoexcitation and hypertension in the elite divers in this study. Nonetheless, the present study is limited by the lack of information on the frequency of near-maximum apneas experienced over time by the elite divers.Of greater significance is the 1-2 month delay between intense apnea training and the day of the study [1]. CIHinduced increases in chemoreceptor sensitivity and sympathetic activity in animal models can be reversed as soon as 10 days after terminating the CIH [17]. Effects of CIH may have dissipated before the divers were studied. On the other hand, the same group of investigators have reported

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Carotid chemoreceptors, systemic blood pressure, and chronic episodic hypoxia mimicking sleep apnea

Cited by 388 publications

References 0 publications

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Carotid sinus nerve stimulation, but not intermittent hypoxia, induces respiratory LTF in adult rats exposed to neonatal intermittent hypoxia

Obstructive sleep apnea syndrome and cardiovascular disease: The influence of C-reactive protein

CIH: from sleep apnea to breath-hold diving

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