Parasympathetic tonic dilatory influences on cerebral vessels

Boysen, Nicholas C.; Dragon, Deidre Nitschke; Talman, William T.

doi:10.1016/j.autneu.2009.01.009

Cited by 24 publications

(15 citation statements)

References 28 publications

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“…Recently, Gourine et al reported that RIPC might be associated with the nerve reflex, which is the sensory afferent pathway from the peripheral organ (limbs) and parasympathetic vagal efferent outflow to the heart in rats [20]. Previous studies showed that there is evidence of parasympathetic vasodilator in the masseter muscle [21], lower lip [22] and brain vessels [23] in animals. Those findings indicated that vasodilatation is a result of reflex via increasing parasympathetic activity.…”

Section: Discussionmentioning

confidence: 98%

Intermittent arm ischemia induces vasodilatation of the contralateral upper limb

et al. 2011

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Intermittent arm ischemia before percutaneous coronary intervention induces remote ischemic preconditioning (RIPC) and attenuates myocardial injury in patients with myocardial infarction. Several studies have shown that intermittent arm ischemia increases coronary flow and is related to autonomic nerve system. The aim of this study was to determine whether intermittent arm ischemia induces vasodilatation of other arteries and to assess changes in the autonomic nerve system during intermittent arm ischemia in humans. We measured change in the right brachial artery diameter during intermittent left arm ischemia through three cycles of 5-min inflation (200 mmHg) and 5-min deflation of a blood-pressure cuff using a 10-MHz linear array transducer probe in 20 healthy volunteers. We simultaneously performed power spectral analysis of heart rate. Ischemia-reperfusion of the left arm significantly dilated the right brachial artery time-dependently, resulting in a 3.2 ± 0.4% increase after the 3rd cycle. In the power spectral analysis of heart rate, the high-frequency domain (HF), which is a marker of parasympathetic activity, was significantly higher after the 3rd cycle of ischemia-reperfusion than baseline HF (P = 0.02). Intermittent arm ischemia was accompanied by vasodilatation of another artery and enhancement of parasympathetic activity. Those effects may play an important role in the mechanism of RIPC.

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Section: Discussionmentioning

confidence: 98%

Intermittent arm ischemia induces vasodilatation of the contralateral upper limb

et al. 2011

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“…Like the sympathetic arm, parasympathetic innervation also displays tonic influence on the cerebrovasculature, but instead acts as a potent vasodilator (50,61,118). However, beyond its tonic role, and importance in certain pathologies [e.g., Alzheimer's (161)], the active parasympathetic contribution to physiological perturbations remains less understood.…”

Section: Neurogenic Regulation Of Cerebral Blood Flowmentioning

confidence: 98%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…This lack of effect is consistent with previous work using this same microinjection technique in which we demonstrated that placements as little as 500 μm away from the RVM had no effect on nocifensor reflexes (Heinricher and Kaplan, 1991; Heinricher et al, 1994). These anatomical controls thus allow us to localize drug action to the RVM (Yaksh and Rudy, 1978; Wise and Hoffman, 1992), and rule out diffusion to brainstem sympathetic and parasympathetic premotor areas previously implicated in regulation of cerebral blood flow, such as the superior salivatory nuclei or rostral ventrolateral medulla (Underwood et al, 1992; Golanov and Reis, 1994; Talman et al, 2007; Boysen et al, 2009). …”

Section: Discussionmentioning

confidence: 99%

Brainstem control of cerebral blood flow and application to acute vasospasm following experimental subarachnoid hemorrhage

et al. 2009

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Symptomatic ischemia following aneurysmal subarachnoid hemorrhage is common but poorly understood and inadequately treated. Severe constriction of the major arteries at the base of the brain, termed vasospasm, traditionally has been thought to be a proximal event underlying these ischemias, although microvascular changes also have been described. The vast majority of studies aimed at understanding the pathogenesis of ischemic deficits and vasospasm have focused on the interaction of the "spasmogen" of the extravasated blood with the smooth muscle and endothelium of the arteries. This has led to a comparative neglect of the contribution of the central nervous system to the maintenance of cerebral perfusion. In the present study, we focused on the role of the rostral ventromedial medulla (RVM) in modulating cerebral perfusion at rest and following an experimental subarachnoid hemorrhage in the rat. Changes in cerebral blood flow (CBF) were measured using laser-Doppler flowmetry and three-dimensional optical microangiography. Focal application of a GABA A receptor agonist and antagonist were used to respectively inactivate and activate the RVM. We show here that the RVM modulates cerebral blood flow under resting conditions, and further, contributes to restoration of cerebral perfusion following a high-grade subarachnoid hemorrhage. Failure of this brainstem compensatory mechanism could be significant for acute perfusion deficits seen in patients following subarachnoid hemorrhage.Keywords cerebral blood flow; subarachnoid hemorrhage; brainstem; modulation Symptomatic ischemic deficits remain poorly understood and inadequately treated sequelae of aneurysmal subarachnoid hemorrhage (SAH), and are seen in 25-30% of patients. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2010 October 6. Published in final edited form as:Neuroscience. Approximately half of those suffer permanent disability or death (Lombard and Borel, 2007). Vasospasm of the major arteries is thought to be a major contributor to the development of cerebral infarcts in these patients, although it is not necessary nor sufficient for all cases of ischemia (Macdonald et al., 2007).The majority of studies on the sequelae of SAH have focused on arterial smooth muscle and endothelium. Abnormal contraction of smooth muscle, free radical release, endothelial factors, nitric oxide, endothelins, inflammatory mediators, neuronal cell death and structural changes in the arterial wall have all been implicated. However, the focus on t...

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Parasympathetic tonic dilatory influences on cerebral vessels

Cited by 24 publications

References 28 publications

Intermittent arm ischemia induces vasodilatation of the contralateral upper limb

Intermittent arm ischemia induces vasodilatation of the contralateral upper limb

Cerebral Vascular Control and Metabolism in Heat Stress

Brainstem control of cerebral blood flow and application to acute vasospasm following experimental subarachnoid hemorrhage

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