Management of aneurysmal subarachnoid hemorrhage.

Biller, José; Godersky, John C.; Adams, Harold P.

doi:10.1161/01.str.19.10.1300

Cited by 146 publications

(48 citation statements)

References 54 publications

(31 reference statements)

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“…Cerebral aneurysms tend to rupture in relatively young individuals (age of peak rupture rate ∼55 y), compounding the societal and economic impact of SAH. Delayed ischemic neurological deficits (DINDs), developing several days after aneurysm rupture, are a significant contributor to morbidity and mortality in SAH patients (2).…”

mentioning

confidence: 99%

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Koide

Bonev

Nelson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

101

108

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The cellular events that cause ischemic neurological damage following aneurysmal subarachnoid hemorrhage (SAH) have remained elusive. We report that subarachnoid blood profoundly impacts communication within the neurovascular unit-neurons, astrocytes, and arterioles-causing inversion of neurovascular coupling. Elevation of astrocytic endfoot Ca 2+ to ∼400 nM by neuronal stimulation or to ∼300 nM by Ca 2+ uncaging dilated parenchymal arterioles in control brain slices but caused vasoconstriction in post-SAH brain slices. Inhibition of K + efflux via astrocytic endfoot large-conductance Ca 2+ -activated K + (BK) channels prevented both neurally evoked vasodilation (control) and vasoconstriction (SAH

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mentioning

confidence: 99%

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Koide

Bonev

Nelson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

101

108

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“…Vasospasm occurs in 70% of patients with aneurysmal SAH and leads to ischemic deficits in 36% of patients (5). Despite extensive investigation, the factors that trigger the decline in cerebral blood flow (CBF) after SAH remain to be determined.…”

mentioning

confidence: 99%

Hemoglobin, NO, and 20-HETE interactions in mediating cerebral vasoconstriction following SAH

Takeuchi¹,

Miyata²,

Renić³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Recent studies have indicated that 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to the fall in cerebral blood flow (CBF) after subarachnoid hemorrhage (SAH), but the factors that stimulate the production of 20-HETE are unknown. This study examines the role of vasoactive factors released by clotting blood vs. the scavenging of nitric oxide (NO) by hemoglobin (Hb) in the fall in CBF after SAH. Intracisternal (icv) injection of blood produced a greater and more prolonged (120 vs. 30 min) decrease in CBF than that produced by a 4% solution of Hb. Pretreating rats with N -nitro-L-arginine methyl ester (L-NAME; 10 mg/kg iv) to block the synthesis of NO had no effect on the fall in CBF produced by an icv injection of blood. L-NAME enhanced rather than attenuated the fall in CBF produced by an icv injection of Hb. Blockade of the synthesis of 20-HETE with TS-011 (0.1 mg/kg iv) prevented the sustained fall in CBF produced by an icv injection of blood and the transient vasoconstrictor response to Hb. Hb (0.1%) reduced the diameter of the basilar artery (BA) of rats in vitro by 10 Ϯ 2%. This response was reversed by TS-011 (100 nM). Pretreatment of vessels with L-NAME (300 M) reduced the diameter of BA and blocked the subsequent vasoconstrictor response to the addition of Hb to the bath. TS-011 returned the diameter of vessels exposed to L-NAME and Hb to that of control. These results suggest that the fall in CBF after SAH is largely due to the release of vasoactive factors by clotting blood rather than the scavenging of NO by Hb and that 20-HETE contributes the vasoconstrictor response of cerebral vessels to both Hb and blood. subarachnoid hemorrhage; nitric oxide; 20-hydroxyeicosatetraenoic acid CEREBRAL VASOSPASM IS A CRITICAL complication of subarachnoid hemorrhage (SAH). Vasospasm occurs in 70% of patients with aneurysmal SAH and leads to ischemic deficits in 36% of patients (5). Despite extensive investigation, the factors that trigger the decline in cerebral blood flow (CBF) after SAH remain to be determined.The fall in CBF after SAH correlates with the amount of hemoglobin (Hb) released into cerebrospinal fluid (CSF), and vasospasm can be triggered by an injection of Hb alone into the CSF (31, 51). Hb induces hemeoxygenase-1 (24) that increases iron levels, which generate superoxide radicals (30). Superoxide radicals at low concentration have been reported to constrict vessels in several vascular beds in part by decreasing the levels of nitric oxide (NO) (13, 42), and there is a recent report that supports a similar mechanism in cerebral arteries (55). Free radicals also increase the production of lipid peroxides and isoprostanes (20, 44) that are potent constrictors of cerebral arteries (19).Previous studies have focused on the role of various vasoconstrictor pathways in the development of cerebral vasospasm. The levels of endothelin (46), thromboxane (36), ATP (31), isoprostanes (44), glutamate (4), platelet-activating factor (PAF) (17) and serotonin (5-HT) (6, 43) in CSF all increase after SAH, and the ...

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“…Subarachnoidhemorrhage (SAH) accounts for about 6-8% of all strokes [1], among which the common cause is rupture of intracerebral aneurysm. The other causes are mainly vertebral artery dissection, arteriovenous malformation bleeding, or due to perimesencephalic SAH and some undefined causes [2].…”

Section: Introductionmentioning

confidence: 99%

CSF S100B in patients treated by endovascular coiling or surgical clipping after aneurysmal subarachnoid hemorrhage and its correlation to cerebral vasospasm

et al. 2017

Chin Neurosurg Jl

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Background: Aneurysmal subarachnoid hemorrhage (aSAH) is an acute neurosurgical emergency with a significant fatality rate. In addition to acute brain injury, a considerable part of patients suffering from aSAH develops secondary brain damage such as cerebral vasospasm (CVS). CVS exacerbates the mortality. Therefore, it is urgently needed to find a biomarker, which could predict secondary brain and lead to operation by physicians more promptly. S100B, produced and released by astrocytes, has proven to be an important biomarker for brain injury. Methods: In this present study, 51 patients with aSAH were included. Five CSF samples from each patient were obtained via lumbar puncture and were detected using electrochemiluminescence immunoassay (ECLIA). Results: It indicated that S100B had a higher concentration in CSF of patients treated by surgical clipping after aSAH than that treated with endovascular coiling. In addition, the mean CSF S100B level in patients without CVS was much lower compared with patients with CVS. And, the expression of S100B increased along with the Fisher Grade at the same day after aSAH attacked and decreased as time went on. Moreover, the CSF S100B level of different time points and the mean CSF S100B level can predict the risk of CVS. Conclusions: These data suggest that CSF S100B can be served as a predictor of CVS, which triggers an immediate management by clinicians to prevent secondary exacerbation.

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Management of aneurysmal subarachnoid hemorrhage.

Cited by 146 publications

References 54 publications

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Hemoglobin, NO, and 20-HETE interactions in mediating cerebral vasoconstriction following SAH

CSF S100B in patients treated by endovascular coiling or surgical clipping after aneurysmal subarachnoid hemorrhage and its correlation to cerebral vasospasm

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Management of aneurysmal subarachnoid hemorrhage.

Cited by 146 publications

References 54 publications

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca 2+ -activated K + (BK) channels

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca 2+ -activated K + (BK) channels

Hemoglobin, NO, and 20-HETE interactions in mediating cerebral vasoconstriction following SAH

CSF S100B in patients treated by endovascular coiling or surgical clipping after aneurysmal subarachnoid hemorrhage and its correlation to cerebral vasospasm

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Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels

Inversion of neurovascular coupling by subarachnoid blood depends on large-conductance Ca ²⁺ -activated K ⁺ (BK) channels