Circulating norepinephrine and cerebrovascular control in conscious humans

Kimmerly, Derek S.; Tutungi, Elli; Wilson, Timothy D.; Serrador, Jorge M.; Gelb, Adrian W.; Hughson, Richard L.; Shoemaker, J. Kevin

doi:10.1046/j.1475-0961.2003.00507.x

Cited by 42 publications

(32 citation statements)

References 39 publications

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“…There have been several studies investigating the effects of amphetamine on CBF. Although different research groups, depending on various measurement techniques, have demonstrated increased (Devous et al 2001;Price et al 2002;Rose et al 2006), as well as decreased (Alhassoon et al 2001;Mathew and Wilson 1989;Polesskaya et al 2011;Wang et al 2001), or unchanged flow (Kimmerly et al 2003) in response to amphetamine, it is mostly assumed in the interpretation of benzamide PET studies that amphetamine induces transient increases in CBF with rapid return to baseline values (Price et al 2002). An amphetamine-induced increase in CBF could increase the delivery of the tracer and we may observe a larger V T , thus possibly underestimating the amphetamineinduced decrease in α2 adrenoceptor binding.…”

Section: Discussionmentioning

confidence: 99%

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

2012

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Section: Discussionmentioning

confidence: 99%

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

2012

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“…NE is the primary neurotransmitter in post-ganglionic sympathetic nerves. However, it is well established that NE infusion has no direct influence on the cerebrovascular tone or CBF [10,17], and we assume that NE mediates its effects through changes in blood pressure. Furthermore, infusion of NE is not known to lead to change in PaCO 2 levels, and thus does not appear to indirectly affect the cerebrovascular tone [21].…”

Section: J Methodological Considerationsmentioning

confidence: 99%

Autonomic dysfunction and impaired cerebral autoregulation in cirrhosis

et al. 2006

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Cerebral blood flow autoregulation is lost in patients with severe liver cirrhosis. The cause of this is unknown. We determined whether autonomic dysfunction was related to impaired cerebral autoregulation in patients with cirrhosis. Fourteen patients with liver cirrhosis and 11 healthy volunteers were recruited. Autonomic function was assessed in response to deep breathing, head-up tilt and during 24-h Holter monitoring. Cerebral autoregulation was assessed by determining the change in mean cerebral blood flow velocity (MCAVm, transcranial Doppler) during an increase in blood pressure induced by norepinephrine infusion (NE). The severity of liver disease was assessed using the Child-Pugh scale (class A, mild; class B, moderate; class C, severe liver dysfunction).NE increased blood pressure similarly in the controls (27 (24-32) mmHg) and patients with the most severe liver cirrhosis (Child-Pugh C, 31 (26-44) mmHg, p=0.405 Mann-Whitney). However, the increase in MCAVm was greater in cirrhosis patients compared to the controls (Child-Pugh C, 26 (24-39) %; controls, 3 (-1.3 to 3) %; respectively, p=0.016, Mann-Whitney). HRV during deep breathing was reduced in the cirrhosis patients (Child-Pugh C, 6.0+/-2.0 bpm) compared to the controls (21.7+/-2.2 bpm, p=0.001, Tukey' test). Systolic blood pressure fell during head-up tilt only in patients with severe cirrhosis. Our results imply that cerebral autoregulation was impaired in the most severe cases of liver cirrhosis, and that those with impaired cerebral autoregulation also had severe parasympathetic and sympathetic autonomic dysfunction. Furthermore, the degree of liver dysfunction was associated with increasing severity of autonomic dysfunction. Although this association is not necessarily causal, we postulate that the loss of sympathetic innervation to the cerebral resistance vessels may contribute to the impairment of cerebral autoregulation in patients with end-stage liver disease.

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“…Indirect support of this proposed neural control feature comes from evidence that infused norepinephrine stimulates ventilation in conscious humans. Specifically, 200 Ìg/kg/min infusions of norepinephrine reduced end tidal CO 2 by F5%, and this hypocapnia was corrected when phentolamine was coinfused with norepinephrine [44] (fig. 2).…”

Section: Neural Regulation Of Peripheral Chemoreceptorsmentioning

confidence: 99%

“…This hyperventilatory response must have been due to enhanced tidal volume, because breathing frequency was maintained at F14 breaths/min. Data were adapted from Kimmerly et al [44]. mains an intriguing hypothesis that has important implications for understanding the concurrent changes in chemoreceptor sensitivity and hyperadrenergic activity in many patient groups.…”

Section: Neurogenic Coupling Of Ventilatory and Autonomic Reflexesmentioning

confidence: 99%

“…Thus, the enhanced ventilation was related to an ·-adrenergic receptor-mediated effect. The apparent inability of infused norepinephrine to influence cerebrovascular control [44] suggests that circulating catecholamines do not influence central chemoreceptor control, but rather exert their effect through the peripheral chemoreceptors. Although this hypothesis requires systematic investigation, it is supported by anatomical evidence that the carotid body receives sympathetic innervation [for a review, see ref.…”

Section: Neural Regulation Of Peripheral Chemoreceptorsmentioning

confidence: 99%

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Peripheral Chemoreceptor Contributions to Cardiovascular Regulation

Shoemaker¹

2004

Heart Drug

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Oxygen homeostasis at the cellular level depends on acute and appropriate cardiovascular adjustments elicited by neural chemosensitive reflexes. This review addresses the integrated physiology of peripheral chemoreflex control of cardiovascular function with emphasis on the relevance for the intact and conscious human. Peripheral chemoreceptor activation affects sympathoexcitatory and cardiovascular responses that can be modified by the concurrent effects of enhanced ventilation. Additional changes in baroreflex control during chemoreceptor activation must be considered in determining chemoreflex-mediated cardiovascular regulation. Moreover, the autonomic response elicited by the peripheral chemoreflex may enhance the sensitivity of these chemoreceptors, further enhancing or prolonging the neural and cardiovascular consequences of hypoxia. Finally, the recent interest in the role of altered chemoreflex sensitivity and function in cardiovascular pathology is highlighted. The collective information suggests that these interactions may contribute importantly to cardiovascular pathology requiring considerable research into the linkage between cellular and genomic mechanisms that affect the integrated systems response in health and disease.

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Circulating norepinephrine and cerebrovascular control in conscious humans

Abstract: The increase in CVR during NE infusion was explained by an autoregulatory response to the increased blood pressure and not an alpha-mediated constriction. However, PHO appeared to interfere with the normal autoregulatory response to increasing blood pressure.

Cited by 42 publications

References 39 publications

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

Amphetamine challenge decreases yohimbine binding to α2 adrenoceptors in Landrace pig brain

Autonomic dysfunction and impaired cerebral autoregulation in cirrhosis

Peripheral Chemoreceptor Contributions to Cardiovascular Regulation

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