Changes in the Efferent Discharges of Sympathetic and Parasympathetic Cardiac Nerves Provoked by Activation of Carotid Chemoreceptors

Alanís, J; Defilló, B.; Gordon, S.

doi:10.3109/13813456809058701

Cited by 7 publications

(3 citation statements)

References 17 publications

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“…Carotid body stimulation provokes a wide array of cardiopulmonary and autonomic reflexes as well as endocrine responses (e.g., plasma release of catecholamines and cortisol) (Fitzgerald, 2014 ). In particular, chemoreflexes are important modulators of sympathetic activation (Abboud and Thames, 1983 ), and peripheral chemoreceptor activation elicits respiratory and cardiovascular effects and a sympatho-excitatory response (Alanis et al, 1968 ; Montarolo et al, 1976 ). Thus, tonic activation of carotid chemoreceptors during sepsis may also contribute to high levels of sympathetic activity (Kara et al, 2003 ).…”

Section: Carotid Body Stimulation As a Target For Sepsis Therapy: Symmentioning

confidence: 99%

Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy

et al. 2014

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Sepsis progresses to multiple organ dysfunction due to the uncontrolled release of inflammatory mediators, and a growing body of evidence shows that neural signals play a significant role in modulating the immune response. Thus, similar toall other physiological systems, the immune system is both connected to and regulated by the central nervous system. The efferent arc consists of the activation of the hypothalamic–pituitary–adrenal axis, sympathetic activation, the cholinergic anti-inflammatory reflex, and the local release of physiological neuromodulators. Immunosensory activity is centered on the production of pro-inflammatory cytokines, signals that are conveyed to the brain through different pathways. The activation of peripheral sensory nerves, i.e., vagal paraganglia by the vagus nerve, and carotid body (CB) chemoreceptors by the carotid/sinus nerve are broadly discussed here. Despite cytokine receptor expression in vagal afferent fibers, pro-inflammatory cytokines have no significant effect on vagus nerve activity. Thus, the CB may be the source of immunosensory inputs and incoming neural signals and, in fact, sense inflammatory mediators, playing a protective role during sepsis. Considering that CB stimulation increases sympathetic activity and adrenal glucocorticoids release, the electrical stimulation of arterial chemoreceptors may be suitable therapeutic approach for regulating systemic inflammation.

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Section: Carotid Body Stimulation As a Target For Sepsis Therapy: Symmentioning

confidence: 99%

Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy

et al. 2014

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“…Thus, there is no consensus about the role played by arterial baroreceptors during sepsis. Classically, the stimulation of peripheral chemoreceptors evokes respiratory and cardiovascular effects and a sympatho-excitatory response (Alanis et al, 1968;Montarolo et al, 1976). Cardiac chemoreflex sensitivity (CCRS) allow us to estimate the sympathetic influence upon cardiorespiratory responses (Schmidt et al, 1999).…”

Section: Pathophysiology Of Sepsis and Multiple Organ Dysfunction Synmentioning

confidence: 99%

Neural Reflex Control of Inflammation During Sepsis Syndromes

Fernández¹,

Acuña-Castillo²

2012

Sepsis - An Ongoing and Significant Challenge

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“…Although it is well known that stimulation of arterial chemoreceptors produces augmentation of respiration and pressor responses, the effects on heart rate are controversial. Some investigators have found that, in anesthetized animals with controlled ventilation, bradycardia is evoked by chemoreceptor stimulation (1)(2)(3)(4). Others have reported that a moderate tachycardia is obtained when chemoreceptors are stimulated (5,6).…”

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confidence: 99%

Nature of differential sympathetic discharges in chemoreceptor reflexes

Kollai¹,

Koizumi²,

Brooks³

1978

Proc. Natl. Acad. Sci. U.S.A.

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In a study of autonomic reflexes it was found that some produce a generalized, bilaterally uniform response whereas others have an asymmetric or laterality of action. Recordings from vertebral nerve fibers (mainly vasoconstrictors to forelimb muscles), right and left cardiac sympathetics, and renal nerves show that baroreceptors evoke a bilaterally uniform inhibition but chemoreceptors of the carotid sinus and aortic arch initiate a differential discharge. In the chemoreceptor reflex the vagi are activated and bradycardia generally occurs. Vertebral and renal sympathetic fibers increase their activity bilaterally commensurate with the increase in arterial pressure. Sympathetic discharges to the heart, however, are not uniform; they show ipsilateral inhibition and a strong contralateral increase in activity. Stabilization of blood pressure or inactivation of baroreceptors abolishes the ipsilateral inhibition. In isolation, therefore, the chemoreceptor-induced cardiac sympathetic discharge is just quantitatively stronger contralaterally. In the absence of vagi, heart rate changes differ depending on which chemoreceptors are stimulated, because the pacemaker is on the right. Asymmetrical discharges do occur and, in the eventual response to stimulation of chemoreceptors, reflex interactions actually augment the laterality of effects. Peripheral interactions, in the sense that changes effected by one may induce another reflex, are responsible in part for the balances of autonomic activity ultimately seen as the body reacts to stimuli.A long-lasting concern of those who study functions of the autonomic nervous system has been to determine how its central control mechanisms can respond to certain stimuli by producing a differential response whereas other stimuli cause the sympathetic division to discharge as a whole. The responses to baroreceptor and chemoreceptor stimulations provide examples of the two categories of effect, and we thought an analysis of their discharge patterns, particularly those evoked by stimulation of the chemoreceptors, would be instructive. Although it is well known that stimulation of arterial chemoreceptors produces augmentation of respiration and pressor responses, the effects on heart rate are controversial. Some investigators have found that, in anesthetized animals with controlled ventilation, bradycardia is evoked by chemoreceptor stimulation (1-4). Others have reported that a moderate tachycardia is obtained when chemoreceptors are stimulated (5, 6).In previous studies (7, 8) we found that stimulation of the carotid chemoreceptors led to a decrease in cardiac sympathetic discharge but an augmentation in the activity of vertebral nerve fibers that have a vasoconstrictor action on vessels of the forelimb. Similar differential discharges have been recorded by others from splanchnic and cardiac sympathetics during chemoreceptor reflexes (9). In further investigations of the mechanisms whereby differential responses of the sympathetic system are evoked, we have identifed two factors ...

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Changes in the Efferent Discharges of Sympathetic and Parasympathetic Cardiac Nerves Provoked by Activation of Carotid Chemoreceptors

Cited by 7 publications

References 17 publications

Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy

Neural reflex regulation of systemic inflammation: potential new targets for sepsis therapy

Neural Reflex Control of Inflammation During Sepsis Syndromes

Nature of differential sympathetic discharges in chemoreceptor reflexes

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