Renal Sympathetic Nerve Activity After Dexmedetomidine in Nerve-Intact and Baroreceptor-Denervated Rabbits

Oku, Satoru; Benson, Kirk T.; Hirakawa, Masahisa; Gotô, Hiroshi

doi:10.1097/00000539-199609000-00006

Cited by 4 publications

(7 citation statements)

References 18 publications

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“…The results of previous studies (Oku et al, 1996; Xu et al, 1998) demonstrate that Dex administration produces renal sympathoinhibition. Whether this represents the selective inhibition of sympathetic outflow to a specific target, or is indicative of a generalized inhibition of sympathetic nerve activity to other targets, in particular other visceral targets, especially the spleen, has remained unknown.…”

Section: Discussionmentioning

confidence: 82%

“…Dex and vehicle were administered as intravenous (iv) bolus doses via a femoral venous catheter. The range of Dex doses was selected based on previous studies in animals (Xu et al, 1998; 10 μg/kg iv: Oku et al, 1996; 3 μg/kg iv) and humans (Kontak et al, 2013; 0.1–1.0 μg/kg iv). Experiments were completed in baroreceptor-intact (intact) and SAD rats.…”

Section: Methodsmentioning

confidence: 99%

“…Alpha 2 -adrenergic receptor agonists influence SND regulation. Intravenous Dex administration reduces renal SND in anesthetized baroreceptor-intact (intact) and baroreceptor-denervated (SAD) rabbits (Oku et al, 1996; Xu et al, 1998), whereas intracerebroventricular Dex administration reduces plasma norepinephrine levels in conscious rats (Shirasaka et al, 2007). In addition, intravenous Dex abolishes cocaine-induced increases in skin SND in conscious humans (Menon et al, 2007; Kontak et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Kenney¹,

Larsen²,

McMurphy³

et al. 2014

Autonomic Neuroscience

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Recent lines of inquiry indicate sedatives can influence the immune system, leading to the concept of sedative-induced immunomodulation. It has been hypothesized that sedatives may alter immune responses by modulating the sympathetic nervous system, however, little information is known regarding the effects of sedatives on regulation of splenic sympathetic nerve discharge (SND), a significant omission based on the functional role that changes in splenic SND exert on splenic cytokine gene expression. The present investigation determined the effect of systemic Dexmedetomidine (Dex) administration on the level of directly-recorded splenic SND and tested the hypothesis that the intravenous administration of Dex would inhibit splenic SND in anesthetized rats. The present results demonstrate for the first time that intravenous Dex administration significantly reduces splenic sympathetic nerve outflow in baroreceptor-intact and sinoaortic-denervated rats, indicating that Dex administration alters the central regulation of splenic SND. The present results provide new information regarding the effect of a centrally-acting alpha2-adrenergic agonist on the level of sympathetic nerve outflow to a secondary lymphoid organ that plays a critical role in peripheral immune responses.

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Section: Discussionmentioning

confidence: 82%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Kenney¹,

Larsen²,

McMurphy³

et al. 2014

Autonomic Neuroscience

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“…α 2 ‐Adrenoceptor agonists reset baroreceptor function and lower blood pressure without reflex tachycardia, but there are conflicting reports on the extent of further interference with baroreceptor function. 6,7 Clonidine, acting via a range of receptors, including α 1 ‐ and α 2 ‐adrenoceptors and imidazoline receptors, may have a greater effect on baroreceptor‐mediated heart rate (HR) and vasoconstrictor reflexes than dexmedetomidine. 8,9 Sudden changes in central blood volume result in dependence on intact baroreceptor‐mediated vasoconstriction to maintain haemodynamic stability during surgery and the perioperative use of clonidine is reported to result in increased interventions to treat hypotension and bradycardia.…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine And Haemodynamic Responses To Acute Central Hypovolaemia In Conscious Rabbits

Ludbrook

Leeuwen

2000

Clin Exp Pharma Physio

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1. Effects of the alpha2-adrenoceptor agonist dexmedetomidine on vasoconstrictor and heart rate (HR) responses to acute central hypovolaemia were studied in eight chronically instrumented rabbits. We compared intravenous (i.v.) and fourth ventricular (V4) dexmedetomidine (0.1-10 microg/kg) and the reversal of effects by the alpha2-adrenoceptor antagonist idazoxan and the opioid agonist alfentanil. 2. Gradual inflation of an inferior vena cava (IVC) cuff reduced cardiac index (CI) by 8%/min, with progressive vasoconstriction and increased HR. In control rabbits, at approximately 40% baseline CI, there was sudden decompensation with failure of vasoconstriction and a fall in mean arterial pressure (MAP). 3. Dexmedetomidine (i.v. and V4) reduced resting MAP and HR and caused an earlier decompensation during central hypovolaemia. Intravenous dexmedetomidine (3 and 10 microg/kg) also reduced the slope of the initial vasoconstrictor response and the maximum HR. 4. The effects of dexmedetomidine were reversed by the antagonist idazoxan, which prevented the decompensation phase. Intravenous alfentanil was also effective in restoring the vasoconstrictor response and delaying decompensation with hypovolaemia after dexmedetomidine. Combining dexmedetomidine with an opioid, such as alfentanil, may provide the benefit of reduced sympathetic tone without increased risk of cardiovascular collapse.

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“…Direct SND recordings provide an output measure of central sympathetic neural circuits and centrally-acting alpha 2 -adrenergic receptor agonists modulate SND. For example, intravenous Dexmedetomidine (Dex) administration abolishes cocaine-induced increases in skin SND in conscious humans (Menon et al, 2007; Kontak et al, 2013), reduces renal SND in anesthetized rabbits (Oku et al, 1996; Xu et al, 1998), and decreases visceral (splenic and renal) SND in young, anesthetized Fischer 344 (F344) rats (Kenney et al, 2014). …”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine and regulation of splenic sympathetic nerve discharge in aged F344 rats

McMurphy¹,

Fels²,

Kenney³

2015

Autonomic Neuroscience

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Sedatives influence the immune system and centrally-acting alpha2-adrenergic receptor agonists, including Dexmedetomidine (Dex), modulate sympathetic nerve discharge (SND). Because sedatives are used under medical conditions that include elderly patients, and because advancing age attenuates SND responsivity to various interventions, we tested the hypothesis that splenic sympathoinhibitory responses to Dex would be attenuated in aged compared with young Fischer 344 rats. Dex-mediated reductions in splenic SND were similar in aged and young baroreceptor-intact and -denervated rats, indicating that SND changes to Dex administration occur in an age-independent manner. These findings provide new information regarding interactions between alpha2-adrenergic agonists, advanced age, and SND regulation.

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Renal Sympathetic Nerve Activity After Dexmedetomidine in Nerve-Intact and Baroreceptor-Denervated Rabbits

Cited by 4 publications

References 18 publications

Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Dexmedetomidine and regulation of splenic sympathetic nerve discharge

Dexmedetomidine And Haemodynamic Responses To Acute Central Hypovolaemia In Conscious Rabbits

Dexmedetomidine and regulation of splenic sympathetic nerve discharge in aged F344 rats

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