Regulation of cerebral blood vessels by humoral and endothelium-dependent mechanisms. Update on humoral regulation of vascular tone.

Faraci, Frank M.; Heistad, Donald D.

doi:10.1161/01.hyp.17.6.917

Cited by 46 publications

(23 citation statements)

References 62 publications

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“…The basic assumption that severe vasospasm would result in impaired blood flow to the affected territory with subsequent development of new infarct, has been tackled by many authors and could not be established [10][11][12]. In our study, although there was significant coincidence between the spastic territory and the location of the new infarcts, however, this assumption is not applicable, as it does not take into consideration the fact that the vasospasm has been interventionally reversed, with subsequent restoration of the normal -or near normal -vessel caliber.…”

Section: Discussionmentioning

confidence: 99%

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Outcome of aneurismal subarachnoid hemorrhage: How far is vasospasm involved? – Retrospective study

Said

El-Ghandour

2015

The Egyptian Journal of Radiology and Nuclear Medicine

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Purpose: To evaluate vasospasm and/or other possible mechanisms as a contributor to poor outcome following aneurismal subarachnoid hemorrhage (SAH). Materials and methods: Sixty patients with aneurismal SAH, and severe cerebral vasospasm warranting endovascular angioplasty were included. Data included age, sex, bleeding severity, number and territory of spastic arteries, angioplasty result, development of new infarcts and their location relative to spastic territory. Final outcome was reported. Results: There was strong correlation between outcome and both grade of hemorrhage and age. Angioplasty was either successful (80%), equivocal (10%), failed (8.3%), or could not be done (1.7%). New Infarcts were found in 44/60 patients (73.3%). In 7 of which (16%) they were out of spastic territory. The remaining 37 (84.1%) had infarcts anatomically related to spasm, of these, 28 had successful angioplasty (75%). No new infarcts were found in the remaining 16 patients (26.7%). There was no significant correlation between new infarcts and either successful angioplasty or outcome. However, when outcome was correlated to infarcts within the spastic territory, it turned strongly significant (p = 0.008). Conclusion: Vasospasm and new infarcts have different pathophysiology. Only the coexistence of both in the same territory significantly correlates with poor outcome. Both are related to severity of SAH.

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Section: Discussionmentioning

confidence: 99%

“…Marked constriction of large cerebral arteries can occur without a decrease in parenchymal CBF [12].…”

Section: Introductionmentioning

confidence: 99%

Outcome of aneurismal subarachnoid hemorrhage: How far is vasospasm involved? – Retrospective study

Said

El-Ghandour

2015

The Egyptian Journal of Radiology and Nuclear Medicine

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“…This suggests that the endothelium-derived NO plays a major role in regulating blood flow and blood pressure. 6 ' 8 The second isoform of NO synthase is constitutively produced in the nervous system, with high concentrations in the neurons of the cerebellum, the olfactory bulb, 9 -11 and the spinal cord 12 - 13 in humans and rats. The distribution of NO synthase in the brain does not parallel that of guanylate cyclase.…”

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confidence: 99%

Spinal cord infarcts during long-term inhibition of nitric oxide synthase in rats.

Blot

Arnal

et al. 1994

Stroke

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Background and Purpose Chronic hypertension is a major predisposing factor for stroke in humans. It has recently been shown that long-term inhibition of nitric oxide synthase activity causes a gradual time-dependent increase in arterial blood pressure in rats. We used this new animal model of chronic hypertension to study the occurrence and spatial features of infarcts in the central nervous system.Methods Rats were treated with a nitric oxide synthase inhibitor, A^°-nitro-L-arginine methyl ester, dissolved in the drinking water at 50 mg/kg per day for 11 weeks. The brains and spinal cords of hypertensive rats with and without motion disturbances were processed for standard microscopic examination.Results Seventy-nine percent of the hypertensive rats showed motion dysfunctions, especially front leg paralysis, and/or died suddenly when their systolic blood pressure reached approximately 215 mm Hg after approximately 7

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“…thelium-derived relaxing factor, i. e., mtnc oxide (NO) or a NO-containing compound (Toda and Okamura, 1990;Faraci and Heistad, 1991). NO is synthesized from L-arginine by NO synthase.…”

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confidence: 99%

Inhibition of Nitric Oxide Synthase Attenuates the Cerebral Blood Flow Response to Stimulation of Postganglionic Parasympathetic Nerves in the Rat

Morita-Tsuzuki

Hardebo

Bouskela

1993

J Cereb Blood Flow Metab

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Summary: Stimulation of cerebrovascular parasympa thetic nerves markedly increases cortical blood flow. Ni tric oxide (NO) or a NO-containing compound is present in these nerves and may therefore, upon release, be partly responsible for the flow increase. In addition, transmit ters released from the nerves may cause synthesis and release of this compound from the endothelium. The contribution of NO synthesis to the cortical blood flow (CoBF) increase during parasympathetic stimulation was elucidated in rat by laser-Doppler flowmetry.Thirty-minute exposure to circulating N w -nitro-L-arginine methyl ester (L-NAME) 50 mg kg-1 eliminated most of the response (from 104 to 8% increase), whereas lO-min The pial arterial tree is innervated by a network of parasympathetic fibers (for review see U ddman and Edvinsson, 1989;Suzuki and Hardebo, 1993). Some of these fibers may extend along branches into the brain parenchyma. Stimulation of the para sympathetic fibers markedly increases the cortical blood flow (CoB F) (see Suzuki and Hardebo, 1993). Upon activation, these fibers may modulate cere bral autoregulation (Koketsu et aI. , 1992; Morita Tsuzuki et aI. , 1993) and suppress infarction volume following cerebral artery occlusion (Kano et aI., 1991; Koketsu et aI., 1992).Acetylcholine, present as transmitter in parasym pathetic nerves (Suzuki et aI. , 1990a), exerts its whole vasodilator action through a release of endoReceived December 16, 1992; final revision received April 12, 1993; accepted May 3, 1993 Address correspondence and reprint requests to Dr. Y. Morita-Tsuzuki at Department of Neurology, Second Tokyo Na tional Hospital, 2-5-Higashigaoka, Meguro-ku, Tokyo 152, Ja pan.Abbreviations used: CoBF, cortical blood flow; MCA, middle cerebral artery; L-NAME, Nw-nitro-L-arginine methyl ester. 993exposure to this dose or 30-min exposure to 5 mg kg -1 caused a less marked reduction. The reducing effect was particularly evident after elimination of the systemic blood pressure increase caused by L-NAME (only 3% increase after the high dose). Infusion of L-arginine re stored the flow response. Resting CoBF was not substan tially affected by blockade of NO formation. Thus, re lease of an NO-containing compound constitutes a major component of the increase in CoBF caused by parasym pathetic nerve stimulation but does not seem to contrib ute to cortical flow regulation during resting conditions.

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Regulation of cerebral blood vessels by humoral and endothelium-dependent mechanisms. Update on humoral regulation of vascular tone.

Cited by 46 publications

References 62 publications

Outcome of aneurismal subarachnoid hemorrhage: How far is vasospasm involved? – Retrospective study

Outcome of aneurismal subarachnoid hemorrhage: How far is vasospasm involved? – Retrospective study

Spinal cord infarcts during long-term inhibition of nitric oxide synthase in rats.

Inhibition of Nitric Oxide Synthase Attenuates the Cerebral Blood Flow Response to Stimulation of Postganglionic Parasympathetic Nerves in the Rat

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