Endothelin-1 and cerebral blood flow in a porcine model

Henze, Dirk; Menzel, M.; Soukup, Jens; Scharf, A.; Holz, Carsten; Németh, Norbert; Hanisch, Frank; Clausen, Tobias

doi:10.1016/j.jocn.2006.05.017

Cited by 4 publications

(2 citation statements)

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“…2). In the brain, vascular smooth muscle tone is closely controlled by endogenous substances, such as nitric oxide (NO; Bailey et al 2009 b ) and prostanoids (Hortobágyi et al 2007), as well as C‐natriuretic peptide (Kobayashi et al 1994) and endothelin‐1 (Henze et al 2007) produced by the neighbouring endothelial and neuronal cells (Fig. 2).…”

Section: Control Of Cbfmentioning

confidence: 99%

“…Abbreviations: ABP, arterial blood pressure; ICP, intracranial pressure; CSF, cerebral spinal fluid; CPP, cerebral perfusion pressure; CBV, cerebral blood volume. tone is closely controlled by endogenous substances, such as nitric oxide (NO; Bailey et al 2009b) and prostanoids (Hortobágyi et al 2007), as well as Cnatriuretic peptide (Kobayashi et al 1994) and endothelin-1 (Henze et al 2007) produced by the neighbouring endothelial and neuronal cells (Fig. 2).…”

Section: Control Of Cbfmentioning

confidence: 99%

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Regulation of cerebral blood flow in mammals during chronic hypoxia: a matter of balance

Ainslie

Ogoh

2010

Experimental Physiology

137

148

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Respiratory-induced changes in the partial pressures of arterial carbon dioxide (P aCO 2 ) and oxygen (P aO 2 ) play a major role in cerebral blood flow (CBF) regulation. Elevations in P aCO 2 (hypercapnia) lead to vasodilatation and increases in CBF, whereas reductions in P aCO 2 (hypocapnia) lead to vasoconstriction and decreases in CBF. A fall in P aO 2 (hypoxia) below a certain threshold (<40-45 mmHg) also produces cerebral vasodilatation. Upon initial exposure to hypoxia, CBF is elevated via a greater relative degree of hypoxia compared with hypocapnia. At this point, hypoxia-induced elevations in blood pressure and loss of cerebral autoregulation, stimulation of neuronal pathways, angiogenesis, release of adenosine, endothelium-derived NO and a variety of autocoids and cytokines are additional factors acting to increase CBF. Following 2-3 days, however, the process of ventilatory acclimatization results in a progressive rise in ventilation, which increases P aO 2 and reduces P aCO 2 , collectively acting to attenuate the initial rise in CBF. Other factors acting to lower CBF include elevations in haematocrit, sympathetic nerve activity and local and endothelium-derived vasoconstrictors. Hypoxia-induced alterations of cerebrovascular reactivity, autoregulation and pulmonary vascular tone may also affect CBF. Thus, the extent of change in CBF during exposure to hypoxia is dependent on the balance between the myriad of vasodilators and constrictors derived from the endothelium, neuronal innervations and perfusion pressure. This review examines the extent and mechanisms by which hypoxia regulates CBF. Particular focus will be given to the marked influence of hypoxia associated with exposure to high altitude and chronic lung disease. The associated implications of these hypoxia-induced integrative alterations for the regulation of CBF are discussed, and future avenues for research are proposed. The partial pressures of arterial carbon dioxide (P aCO 2 ) and oxygen (P aO 2 ) play a major role in cerebral blood flow (CBF) regulation. Whilst the role of P aCO 2 in the regulation of CBF has been well described (Ainslie & Duffin, 2009), the influence of hypoxia in the regulation of the cerebral circulation has received little focus, especially in humans. This is somewhat surprising given the development of arterial hypoxaemia in both 'normal' physiological endeavours, such as exercise and ascent to high altitude (HA), and during pathology (e.g. chronic lung disease and heart failure). It has been well reported that hypoxia, reflected in a fall in P aO 2 below a certain threshold (<40-45 mmHg), produces cerebral vasodilatation. The mechanisms underling these responses of hypoxia upon CBF, appearing simple at first, are highly complex and involve interactions of many physiological, metabolic and biochemical processes. The major factors underlying the extent of change in CBF during exposure to reductions in P aO 2 are depicted in Fig. 1. These factors, with particular focus on the integrative mechanisms linking reducti...

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