The Experts below are selected from a list of 234 Experts worldwide ranked by ideXlab platform
Silvia V Conde - One of the best experts on this subject based on the ideXlab platform.
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electrostimulation of the Carotid Sinus Nerve in mice attenuates inflammation via glucocorticoid receptor on myeloid immune cells
Journal of Neuroinflammation, 2020Co-Authors: Aidan Falvey, Silvia V Conde, Fabrice Duprat, Thomas Simon, Sandrine Huguesascery, Nicolas Glaichenhaus, Philippe BlancouAbstract:The Carotid bodies and baroreceptors are sensors capable of detecting various physiological parameters that signal to the brain via the afferent Carotid Sinus Nerve for physiological adjustment by efferent pathways. Because receptors for inflammatory mediators are expressed by these sensors, we and others have hypothesised they could detect changes in pro-inflammatory cytokine blood levels and eventually trigger an anti-inflammatory reflex. To test this hypothesis, we surgically isolated the Carotid Sinus Nerve and implanted an electrode, which could deliver an electrical stimulation package prior and following a lipopolysaccharide injection. Subsequently, 90 min later, blood was extracted, and cytokine levels were analysed. Here, we found that Carotid Sinus Nerve electrical stimulation inhibited lipopolysaccharide-induced tumour necrosis factor production in both anaesthetised and non-anaesthetised conscious mice. The anti-inflammatory effect of Carotid Sinus Nerve electrical stimulation was so potent that it protected conscious mice from endotoxaemic shock-induced death. In contrast to the mechanisms underlying the well-described vagal anti-inflammatory reflex, this phenomenon does not depend on signalling through the autonomic nervous system. Rather, the inhibition of lipopolysaccharide-induced tumour necrosis factor production by Carotid Sinus Nerve electrical stimulation is abolished by surgical removal of the adrenal glands, by treatment with the glucocorticoid receptor antagonist mifepristone or by genetic inactivation of the glucocorticoid gene in myeloid cells. Further, Carotid Sinus Nerve electrical stimulation increases the spontaneous discharge activity of the hypothalamic paraventricular nucleus leading to enhanced production of corticosterone. Carotid Sinus Nerve electrostimulation attenuates inflammation and protects against lipopolysaccharide-induced endotoxaemic shock via increased corticosterone acting on the glucocorticoid receptor of myeloid immune cells. These results provide a rationale for the use of Carotid Sinus Nerve electrostimulation as a therapeutic approach for immune-mediated inflammatory diseases.
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decoding neural metabolic markers from the Carotid Sinus Nerve in a type 2 diabetes model
International Conference of the IEEE Engineering in Medicine and Biology Society, 2019Co-Authors: Marina Cracchiolo, Joana F Sacramento, Silvia V Conde, Alberto Mazzoni, Alessandro Panarese, J Carpaneto, Silvestro MiceraAbstract:Recent studies showed that the Carotid Sinus Nerve (CSN) and the sympathetic nervous system (SNS) are overactivated in type 2 diabetes and that restoring the correct CSN neural activity can re-establish the proper metabolism. However, a robust characterization of the relationship between CSN and SNS neural activities and metabolism in type 2 diabetes is still missing. Here, we investigated the relationship between neural activity of CSN and SNS in control rats and in rats with diet-induced type 2 diabetes and the animal condition during metabolic challenges. We found that the diabetic condition can be discriminated on the basis of CSN and SNS neural activities due to a high-frequency shift in both spectra. This shift is suppressed in the SNS in case of CSN denervation, confirming the role of CSN in driving sympathetic overactivation in type 2 diabetes. Interestingly, the Inter-Burst-Intervals (IBIs) calculated from CSN bursts strongly correlate with perturbations in glycaemia levels. This finding, held for both control and diabetic rats, indicates the possibility of detecting metabolic information from neural recordings even in pathological conditions. Our results suggest that CSN activity could serve as a marker to monitor glycaemic alterations and, therefore, it could be used for closed-loop control of CSN neuromodulation. This paves the way to the development of novel and effective bioelectronic therapies for type 2 diabetes.
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high frequency shift in Carotid Sinus Nerve and sympathetic Nerve activity in type 2 diabetic rat model
International IEEE EMBS Conference on Neural Engineering, 2019Co-Authors: Marina Cracchiolo, Joana F Sacramento, Silvia V Conde, Alberto Mazzoni, Alessandro Panarese, J Carpaneto, Silvestro MiceraAbstract:Overactivity of the sympathetic nervous system (SNS) is associated to several cardiovascular and metabolic dysfunctions, such as hypertension and insulin resistance. Indirect biochemical measurements and surgical manipulations have provided preliminary evidences about a crucial role of the Carotid Sinus Nerve (CSN) in generating the SNS overactivity. However, CSN and SNS neural activities and their interplay have not been yet characterized in healthy and pathological conditions. Understanding this relationship is key for the development of electroceutical approaches to deliver therapeutic neuromodulation to the autonomic nervous system and restore insulin sensitivity. Here we show that early type 2 diabetes rats present a high frequency shift in both CSN and SNS neural activities with respect to control animals. This feature could be an important neural signature characterizing type 2 diabetes. Moreover, we show that CSN resection in early type 2 diabetes rats abolishes SNS high frequency shift confirming that normal SNS activity and insulin sensitivity may be recovered by CSN activity suppression. These findings shed new light on the pathological neural changes within the autonomic nervous system in type 2 diabetes. Moreover, they pave the way for electrical monitoring of the metabolic state of diabetic patients, a key first step for the development of electroceutical therapies.
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high fat diet blunts the effects of leptin on ventilation and on Carotid body activity
The Journal of Physiology, 2018Co-Authors: Maria J Ribeiro, Joana F Sacramento, Teresa Gallegomartin, Elena Olea, Bernardete F Melo, Maria P Guarino, Sara Yubero, Ana Obeso, Silvia V CondeAbstract:KEY POINTS: Leptin plays a role in the control of breathing, acting mainly on central nervous system; however, leptin receptors have been recently shown to be expressed in the Carotid body (CB), and this finding suggests a physiological role for leptin in the regulation of CB function. Leptin increases minute ventilation in both basal and hypoxic conditions in rats. It increases the frequency of Carotid Sinus Nerve discharge in basal conditions, as well as the release of adenosine from the CB. However, in a metabolic syndrome animal model, the effects of leptin in ventilatory control, Carotid Sinus Nerve activity and adenosine release by the CB are blunted. Although leptin may be involved in triggering CB overactivation in initial stages of obesity and dysmetabolism, resistance to leptin signalling and blunting of responses develops in metabolic syndrome animal models. ABSTRACT: Leptin plays a role in the control of breathing, acting mainly on central nervous system structures. Leptin receptors are expressed in the Carotid body (CB) and this finding has been associated with a putative physiological role of leptin in the regulation of CB function. Since, the CBs are implicated in energy metabolism, here we tested the effects of different concentrations of leptin administration on ventilatory parameters and on Carotid Sinus Nerve (CSN) activity in control and high-fat (HF) diet fed rats, in order to clarify the role of leptin in ventilation control in metabolic disease states. We also investigated the expression of leptin receptors and the neurotransmitters involved in leptin signalling in the CBs. We found that in non-disease conditions, leptin increases minute ventilation in both basal and hypoxic conditions. However, in the HF model, the effect of leptin in ventilatory control is blunted. We also observed that HF rats display an increased frequency of CSN discharge in basal conditions that is not altered by leptin, in contrast to what is observed in control animals. Leptin did not modify intracellular Ca2+ in CB chemoreceptor cells, but it produced an increase in the release of adenosine from the whole CB. We conclude that CBs represent an important target for leptin signalling, not only to coordinate peripheral ventilatory chemoreflexive drive, but probably also to modulate metabolic variables. We also concluded that leptin signalling is mediated by adenosine release and that HF diets blunt leptin responses in the CB, compromising ventilatory adaptation.
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Carotid Body Denervation Prevents the Development of Insulin Resistance and Hypertension Induced by Hypercaloric Diets
2016Co-Authors: Emília C. Monteiro, Silvia V CondeAbstract:Increased sympathetic activity is a well-known pathophysiolog-ical mechanism in insulin resistance (IR) and hypertension (HT). The Carotid bodies (CB) are peripheral chemoreceptors that classically respond to hypoxia by increasing chemosensory activity in the Carotid Sinus Nerve (CSN), causing hyperventila-tion and activation of the sympathoadrenal system. Besides its role in the control of ventilation, the CB has been proposed as a glucose sensor implicated in the control of energy homeostasis. However, to date no studies have anticipated its role in the development of IR. Herein, we propose that CB overstimulation is involved in the etiology of IR and HT, core metabolic and hemodynamic disturbances of highly prevalent diseases like the metabolic syndrome, type 2 diabetes, and obstructive sleep apnoea. We demonstrate that CB activity is increased in IR animal models and that CSN resection prevents CB overactiva
Maria P Guarino - One of the best experts on this subject based on the ideXlab platform.
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high fat diet blunts the effects of leptin on ventilation and on Carotid body activity
The Journal of Physiology, 2018Co-Authors: Maria J Ribeiro, Joana F Sacramento, Teresa Gallegomartin, Elena Olea, Bernardete F Melo, Maria P Guarino, Sara Yubero, Ana Obeso, Silvia V CondeAbstract:KEY POINTS: Leptin plays a role in the control of breathing, acting mainly on central nervous system; however, leptin receptors have been recently shown to be expressed in the Carotid body (CB), and this finding suggests a physiological role for leptin in the regulation of CB function. Leptin increases minute ventilation in both basal and hypoxic conditions in rats. It increases the frequency of Carotid Sinus Nerve discharge in basal conditions, as well as the release of adenosine from the CB. However, in a metabolic syndrome animal model, the effects of leptin in ventilatory control, Carotid Sinus Nerve activity and adenosine release by the CB are blunted. Although leptin may be involved in triggering CB overactivation in initial stages of obesity and dysmetabolism, resistance to leptin signalling and blunting of responses develops in metabolic syndrome animal models. ABSTRACT: Leptin plays a role in the control of breathing, acting mainly on central nervous system structures. Leptin receptors are expressed in the Carotid body (CB) and this finding has been associated with a putative physiological role of leptin in the regulation of CB function. Since, the CBs are implicated in energy metabolism, here we tested the effects of different concentrations of leptin administration on ventilatory parameters and on Carotid Sinus Nerve (CSN) activity in control and high-fat (HF) diet fed rats, in order to clarify the role of leptin in ventilation control in metabolic disease states. We also investigated the expression of leptin receptors and the neurotransmitters involved in leptin signalling in the CBs. We found that in non-disease conditions, leptin increases minute ventilation in both basal and hypoxic conditions. However, in the HF model, the effect of leptin in ventilatory control is blunted. We also observed that HF rats display an increased frequency of CSN discharge in basal conditions that is not altered by leptin, in contrast to what is observed in control animals. Leptin did not modify intracellular Ca2+ in CB chemoreceptor cells, but it produced an increase in the release of adenosine from the whole CB. We conclude that CBs represent an important target for leptin signalling, not only to coordinate peripheral ventilatory chemoreflexive drive, but probably also to modulate metabolic variables. We also concluded that leptin signalling is mediated by adenosine release and that HF diets blunt leptin responses in the CB, compromising ventilatory adaptation.
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bioelectronic modulation of Carotid Sinus Nerve activity in the rat a potential therapeutic approach for type 2 diabetes
Diabetologia, 2018Co-Authors: Joana F Sacramento, Bernardete F Melo, Maria P Guarino, Daniel J Chew, Matteo Donega, Wesley Dopson, Alison Robinson, Jesus Prietolloret, Sonal PatelAbstract:Aims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual Nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid Sinus Nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents.
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bioelectronic modulation of Carotid Sinus Nerve activity in the rat a potential therapeutic approach for type 2 diabetes
Diabetologia, 2018Co-Authors: Joana F Sacramento, Bernardete F Melo, Maria P Guarino, Daniel J Chew, Matteo Donega, Wesley Dopson, Alison Robinson, Jesus Prietolloret, Sonal PatelAbstract:A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual Nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid Sinus Nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents. Rats were fed either a chow or high-fat/high-sucrose (HFHSu) diet (60% lipid-rich diet plus 35% sucrose drinking water) over 14 weeks. Neural interfaces were bilaterally implanted in the CSNs and attached to an external pulse generator. The rats were then randomised to KHFAC or sham modulation groups. KHFAC modulation variables were defined acutely by respiratory and cardiac responses to hypoxia (10% O2 + 90% N2). Insulin sensitivity was evaluated periodically through an ITT and glucose tolerance by an OGTT. KHFAC modulation of the CSN, applied over 9 weeks, restored insulin sensitivity (constant of the insulin tolerance test [KITT] HFHSu sham, 2.56 ± 0.41% glucose/min; KITT HFHSu KHFAC, 5.01 ± 0.52% glucose/min) and glucose tolerance (AUC HFHSu sham, 1278 ± 20.36 mmol/l × min; AUC HFHSu KHFAC, 1054.15 ± 62.64 mmol/l × min) in rat models of type 2 diabetes. Upon cessation of KHFAC, insulin resistance and glucose intolerance returned to normal values within 5 weeks. KHFAC modulation of the CSN improves metabolic control in rat models of type 2 diabetes. These positive outcomes have significant translational potential as a novel therapeutic modality for the purpose of treating metabolic diseases in humans.
Joana F Sacramento - One of the best experts on this subject based on the ideXlab platform.
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decoding neural metabolic markers from the Carotid Sinus Nerve in a type 2 diabetes model
International Conference of the IEEE Engineering in Medicine and Biology Society, 2019Co-Authors: Marina Cracchiolo, Joana F Sacramento, Silvia V Conde, Alberto Mazzoni, Alessandro Panarese, J Carpaneto, Silvestro MiceraAbstract:Recent studies showed that the Carotid Sinus Nerve (CSN) and the sympathetic nervous system (SNS) are overactivated in type 2 diabetes and that restoring the correct CSN neural activity can re-establish the proper metabolism. However, a robust characterization of the relationship between CSN and SNS neural activities and metabolism in type 2 diabetes is still missing. Here, we investigated the relationship between neural activity of CSN and SNS in control rats and in rats with diet-induced type 2 diabetes and the animal condition during metabolic challenges. We found that the diabetic condition can be discriminated on the basis of CSN and SNS neural activities due to a high-frequency shift in both spectra. This shift is suppressed in the SNS in case of CSN denervation, confirming the role of CSN in driving sympathetic overactivation in type 2 diabetes. Interestingly, the Inter-Burst-Intervals (IBIs) calculated from CSN bursts strongly correlate with perturbations in glycaemia levels. This finding, held for both control and diabetic rats, indicates the possibility of detecting metabolic information from neural recordings even in pathological conditions. Our results suggest that CSN activity could serve as a marker to monitor glycaemic alterations and, therefore, it could be used for closed-loop control of CSN neuromodulation. This paves the way to the development of novel and effective bioelectronic therapies for type 2 diabetes.
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high frequency shift in Carotid Sinus Nerve and sympathetic Nerve activity in type 2 diabetic rat model
International IEEE EMBS Conference on Neural Engineering, 2019Co-Authors: Marina Cracchiolo, Joana F Sacramento, Silvia V Conde, Alberto Mazzoni, Alessandro Panarese, J Carpaneto, Silvestro MiceraAbstract:Overactivity of the sympathetic nervous system (SNS) is associated to several cardiovascular and metabolic dysfunctions, such as hypertension and insulin resistance. Indirect biochemical measurements and surgical manipulations have provided preliminary evidences about a crucial role of the Carotid Sinus Nerve (CSN) in generating the SNS overactivity. However, CSN and SNS neural activities and their interplay have not been yet characterized in healthy and pathological conditions. Understanding this relationship is key for the development of electroceutical approaches to deliver therapeutic neuromodulation to the autonomic nervous system and restore insulin sensitivity. Here we show that early type 2 diabetes rats present a high frequency shift in both CSN and SNS neural activities with respect to control animals. This feature could be an important neural signature characterizing type 2 diabetes. Moreover, we show that CSN resection in early type 2 diabetes rats abolishes SNS high frequency shift confirming that normal SNS activity and insulin sensitivity may be recovered by CSN activity suppression. These findings shed new light on the pathological neural changes within the autonomic nervous system in type 2 diabetes. Moreover, they pave the way for electrical monitoring of the metabolic state of diabetic patients, a key first step for the development of electroceutical therapies.
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high fat diet blunts the effects of leptin on ventilation and on Carotid body activity
The Journal of Physiology, 2018Co-Authors: Maria J Ribeiro, Joana F Sacramento, Teresa Gallegomartin, Elena Olea, Bernardete F Melo, Maria P Guarino, Sara Yubero, Ana Obeso, Silvia V CondeAbstract:KEY POINTS: Leptin plays a role in the control of breathing, acting mainly on central nervous system; however, leptin receptors have been recently shown to be expressed in the Carotid body (CB), and this finding suggests a physiological role for leptin in the regulation of CB function. Leptin increases minute ventilation in both basal and hypoxic conditions in rats. It increases the frequency of Carotid Sinus Nerve discharge in basal conditions, as well as the release of adenosine from the CB. However, in a metabolic syndrome animal model, the effects of leptin in ventilatory control, Carotid Sinus Nerve activity and adenosine release by the CB are blunted. Although leptin may be involved in triggering CB overactivation in initial stages of obesity and dysmetabolism, resistance to leptin signalling and blunting of responses develops in metabolic syndrome animal models. ABSTRACT: Leptin plays a role in the control of breathing, acting mainly on central nervous system structures. Leptin receptors are expressed in the Carotid body (CB) and this finding has been associated with a putative physiological role of leptin in the regulation of CB function. Since, the CBs are implicated in energy metabolism, here we tested the effects of different concentrations of leptin administration on ventilatory parameters and on Carotid Sinus Nerve (CSN) activity in control and high-fat (HF) diet fed rats, in order to clarify the role of leptin in ventilation control in metabolic disease states. We also investigated the expression of leptin receptors and the neurotransmitters involved in leptin signalling in the CBs. We found that in non-disease conditions, leptin increases minute ventilation in both basal and hypoxic conditions. However, in the HF model, the effect of leptin in ventilatory control is blunted. We also observed that HF rats display an increased frequency of CSN discharge in basal conditions that is not altered by leptin, in contrast to what is observed in control animals. Leptin did not modify intracellular Ca2+ in CB chemoreceptor cells, but it produced an increase in the release of adenosine from the whole CB. We conclude that CBs represent an important target for leptin signalling, not only to coordinate peripheral ventilatory chemoreflexive drive, but probably also to modulate metabolic variables. We also concluded that leptin signalling is mediated by adenosine release and that HF diets blunt leptin responses in the CB, compromising ventilatory adaptation.
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bioelectronic modulation of Carotid Sinus Nerve activity in the rat a potential therapeutic approach for type 2 diabetes
Diabetologia, 2018Co-Authors: Joana F Sacramento, Bernardete F Melo, Maria P Guarino, Daniel J Chew, Matteo Donega, Wesley Dopson, Alison Robinson, Jesus Prietolloret, Sonal PatelAbstract:Aims/hypothesis A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual Nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid Sinus Nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents.
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bioelectronic modulation of Carotid Sinus Nerve activity in the rat a potential therapeutic approach for type 2 diabetes
Diabetologia, 2018Co-Authors: Joana F Sacramento, Bernardete F Melo, Maria P Guarino, Daniel J Chew, Matteo Donega, Wesley Dopson, Alison Robinson, Jesus Prietolloret, Sonal PatelAbstract:A new class of treatments termed bioelectronic medicines are now emerging that aim to target individual Nerve fibres or specific brain circuits in pathological conditions to repair lost function and reinstate a healthy balance. Carotid Sinus Nerve (CSN) denervation has been shown to improve glucose homeostasis in insulin-resistant and glucose-intolerant rats; however, these positive effects from surgery appear to diminish over time and are heavily caveated by the severe adverse effects associated with permanent loss of chemosensory function. Herein we characterise the ability of a novel bioelectronic application, classified as kilohertz frequency alternating current (KHFAC) modulation, to suppress neural signals within the CSN of rodents. Rats were fed either a chow or high-fat/high-sucrose (HFHSu) diet (60% lipid-rich diet plus 35% sucrose drinking water) over 14 weeks. Neural interfaces were bilaterally implanted in the CSNs and attached to an external pulse generator. The rats were then randomised to KHFAC or sham modulation groups. KHFAC modulation variables were defined acutely by respiratory and cardiac responses to hypoxia (10% O2 + 90% N2). Insulin sensitivity was evaluated periodically through an ITT and glucose tolerance by an OGTT. KHFAC modulation of the CSN, applied over 9 weeks, restored insulin sensitivity (constant of the insulin tolerance test [KITT] HFHSu sham, 2.56 ± 0.41% glucose/min; KITT HFHSu KHFAC, 5.01 ± 0.52% glucose/min) and glucose tolerance (AUC HFHSu sham, 1278 ± 20.36 mmol/l × min; AUC HFHSu KHFAC, 1054.15 ± 62.64 mmol/l × min) in rat models of type 2 diabetes. Upon cessation of KHFAC, insulin resistance and glucose intolerance returned to normal values within 5 weeks. KHFAC modulation of the CSN improves metabolic control in rat models of type 2 diabetes. These positive outcomes have significant translational potential as a novel therapeutic modality for the purpose of treating metabolic diseases in humans.
F Marchal - One of the best experts on this subject based on the ideXlab platform.
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Carotid Sinus Nerve chemosensory response to dopamine and acetylcholine in catecholamine depleted cats
Respiratory Physiology & Neurobiology, 2003Co-Authors: Aida Bairam, F MarchalAbstract:Abstract The aim of this study was to determine the role of endogenous dopamine (DA) and the combined effect of DA and acetylcholine (ACh) on the Carotid Sinus Nerve chemosensory discharge (CSND). CSND was measured in vivo in 6 control cats and 6 cats pre-treated with reserpine and alpha-methyl-paratyrosine [catecholamine depleted group: CAD] during infusions of DA and DA+ACh. In normoxia, CSND was similar between CAD's and controls. DA induced CSND depression was transient in controls but sustained in CAD's. Addition of ACh increased CSND in both groups. In hypoxia (8% O 2 in N 2 ), the dynamic CSND response was slowed by DA in CAD's but not controls. Addition of ACh increased this response in both groups. Neither DA nor DA+ACh altered the steady state hypoxic CSND in either group. It is concluded that endogenous DA is important in expressing the dynamic characteristics of both the response to exogenous DA and the response to hypoxia under constant DA infusion. The study also confirms the opposing effects of exogenous DA and ACh on the normoxic CSND.
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effects of caffeine on Carotid Sinus Nerve chemosensory discharge in kittens and cats
Journal of Applied Physiology, 1997Co-Authors: Aida Bairam, P De Grandpre, Charles Dauphin, F MarchalAbstract:Bairam, A., P. De Grandpre, C. Dauphin, and F. Marchal. Effects of caffeine on Carotid Sinus Nerve chemosensory discharge in kittens and cats. J. Appl. Physiol. 82(2): 413–418, 1997.—Caffeine (C) d...
Aida Bairam - One of the best experts on this subject based on the ideXlab platform.
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Carotid Sinus Nerve stimulation but not intermittent hypoxia induces respiratory ltf in adult rats exposed to neonatal intermittent hypoxia
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2010Co-Authors: Cecile Julien, Aida Bairam, Lalah M Niane, Richard Kinkead, Vincent JosephAbstract: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.
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Carotid Sinus Nerve chemosensory response to dopamine and acetylcholine in catecholamine depleted cats
Respiratory Physiology & Neurobiology, 2003Co-Authors: Aida Bairam, F MarchalAbstract:Abstract The aim of this study was to determine the role of endogenous dopamine (DA) and the combined effect of DA and acetylcholine (ACh) on the Carotid Sinus Nerve chemosensory discharge (CSND). CSND was measured in vivo in 6 control cats and 6 cats pre-treated with reserpine and alpha-methyl-paratyrosine [catecholamine depleted group: CAD] during infusions of DA and DA+ACh. In normoxia, CSND was similar between CAD's and controls. DA induced CSND depression was transient in controls but sustained in CAD's. Addition of ACh increased CSND in both groups. In hypoxia (8% O 2 in N 2 ), the dynamic CSND response was slowed by DA in CAD's but not controls. Addition of ACh increased this response in both groups. Neither DA nor DA+ACh altered the steady state hypoxic CSND in either group. It is concluded that endogenous DA is important in expressing the dynamic characteristics of both the response to exogenous DA and the response to hypoxia under constant DA infusion. The study also confirms the opposing effects of exogenous DA and ACh on the normoxic CSND.
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effects of caffeine on Carotid Sinus Nerve chemosensory discharge in kittens and cats
Journal of Applied Physiology, 1997Co-Authors: Aida Bairam, P De Grandpre, Charles Dauphin, F MarchalAbstract:Bairam, A., P. De Grandpre, C. Dauphin, and F. Marchal. Effects of caffeine on Carotid Sinus Nerve chemosensory discharge in kittens and cats. J. Appl. Physiol. 82(2): 413–418, 1997.—Caffeine (C) d...