Delayed postoperative neurological deterioration from prolonged sodium nitroprusside administration

Ram, Zvi; Spiegelman, Roberto; Findler, Gideon; Hadani, Moshe

doi:10.3171/jns.1989.71.4.0605

Cited by 16 publications

(7 citation statements)

References 12 publications

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“…But its effectiveness needs to be confirmed clinically. Furthermore, the longterm therapy (2-3 weeks) with SNAP resulted in cyanide toxicity 80 . We have also tried intravenous delivery of a newly developed NO donor 82 , which spontaneously releases NO and has an extremely short half life (1.8 seconds).…”

Section: No Delivery: Systemicmentioning

confidence: 99%

Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Pluta

2006

Neurological Research

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Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels. It dilates the arteries in response to shear stress, metabolic demands, pterygopalatine ganglion stimulation and chemoregulation. Subarachnoid hemorrhage (SAH) interrupts this regulation of cerebral blood flow. Hemoglobin, gradually released from erythrocytes in the subarachnoid space, destroys nNOS-containing neurons in the conductive arteries. This deprives the arteries of NO, leading to initiation of delayed vasospasm. But such vessel narrowing increases shear stress, which stimulates eNOS. This mechanism normally would lead to increased production of NO and dilation of arteries. However, a transient eNOS dysfunction evoked by an increase in the endogenous competitive NOS inhibitor, asymmetric dimethylarginine (ADMA), prevents this vasodilation. eNOS dysfunction has been recently shown to be evoked by increased levels of ADMA in cerebrospinal fluid (CSF) in response to the presence of bilirubin-oxidized fragments (BOXes). A direct cause of the increased ADMA CSF level is most likely decreased ADMA elimination owing to disappearance of ADMA-hydrolyzing enzyme [dimethylarginine dimethylaminohydrolase II (DDAH II)] immunoreactivity in the arteries in spasm. This eNOS dysfunction sustains vasospasm. CSF ADMA levels are closely associated with the degree and time course of vasospasm; when CSF ADMA levels decrease, vasospasm resolves. Thus, exogenous delivery of NO, inhibiting the L-arginine-methylating enzyme or stimulating DDAH II, may provide new therapeutic modalities to prevent and treat vasospasm. This paper will present results of pre-clinical studies supporting the NO-based hypothesis of delayed cerebral vasospasm development and its prevention by increased NO availability.

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Section: No Delivery: Systemicmentioning

confidence: 99%

Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Pluta

2006

Neurological Research

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“…When used clinically to treat emergency hypertension, sodium nitroprusside sometimes causes delayed neurodegeneration (Kim et al, 1982;Ram et al, 1989), which may be related to the toxicity observed in cultured cerebellar granule neurons treated with nitroprusside as shown in this study. The mechanisms underlying sodium nitroprusside neurotoxicity are complex, possibly involving lowering of [Ca 2~], (present study), inhibition of excitatory amino acidinduced phosphoinositide hydrolysis (Yu and Chuang, 1995), NO cascade (Dawson et al, 1991;Gross, 1995), and/or the actions of the breakdown products of sodium nitroprusside such as cyanide and iron.…”

Section: Rescuing Effects On Neurons By Neurotrophinsmentioning

confidence: 57%

Neurotrophin Protection Against Toxicity Induced by Low Potassium and Nitroprusside in Cultured Cerebellar Granule Neurons

Chuang

1997

Journal of Neurochemistry

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Long‐term survival of cultured rat cerebellar granule neurons requires depolarizing concentrations of potassium (high potassium; 25 mM KCl). A high‐potassium culturing condition has been reported to increase the intracellular calcium concentration ([Ca2+]i) and the expression of brain‐derived neurotrophic factor (BDNF), which in turn induces the expression of neurotrophin‐3 (NT‐3) in these neurons. We therefore examined the neurotrophic effect of these two neurotrophins in low‐potassium (5 mM) cultures and their neuroprotective capabilities against sodium nitroprusside‐induced neurotoxicity in both low‐ and high‐potassium cultures. Neuronal survival and neurotrophic effects were monitored by [3H]ouabain binding and 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assays. In low‐potassium cultures, the neurotrophic effect of BDNF approached that found in high‐potassium cultures but was much more robust than that of NT‐3. In contrast, undifferentiated neurons cultured in high‐potassium medium were much less responsive to BDNF and not responsive at all to NT‐3. Induction of nitroprusside neurotoxicity occurred more readily in low‐ than in high‐potassium cultures. BDNF, NT‐3, and a high potassium concentration, alone or in combination, were unable to protect neurons treated with nitroprusside at 50 or 100 µM. However, the neurotoxicity of a lower dose of nitroprusside (10 µM) was reversed by the combined actions of these two neurotrophins in low‐potassium cultures and by BDNF alone in high‐potassium cultures. Because nitroprusside neurotoxicity is less robust in high‐potassium cultures, high‐potassium‐induced BDNF expression and subsequent NT‐3 expression may participate in its neuroprotection and neurotrophism in these cultures. Also, we found that toxic doses of nitroprusside antagonized KCl‐ and NMDA‐induced rises in [Ca2+]i, suggesting that this effect is related to nitroprusside‐induced neurotoxicity.

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“…23) However, the feasibility of continuous use remains unclear, as cyanide poisoning and cyanide encephalopathy are possible, even at low doses. 21) Higher doses of intravenous nitroglycerin are necessary for the treatment of cerebral vasospasm, which may affect mean arterial pressure. 2,12) Moreover, thiols are essential for the biotransformation of nitroglycerin or other nitrates to generate NO, so depletion of thiols results in development of tolerance.…”

Section: Discussionmentioning

confidence: 99%

In Vitro Effects of New Generation Fungal Derived Nitric Oxide Donors on Rabbit Basilar Artery

Islam

Ohkuma

Kimura

et al. 2003

Neurol. Med. Chir.(Tokyo)

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The fungal derived nitric oxide donors, (E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide (FK409) and N-[(E)-4-ethyl-3-[(Z)-hydroxyimino]-5-nitro-3-hexen-1-yl]-3-pyridinecarboxamide (FR144420), were evaluated for the treatment and prevention of cerebral vasospasm induced by subarachnoid hemorrhage (SAH) by an in vitro study using rabbit basilar artery. The tension-relaxation of a 3 mm-long artery segment was carried out in a micro-tissue organ bath with a real-time recorder to record the tension-relaxation curve. Steady contraction of the specimens was induced by KCl (n ＝ 12) and oxyhemoglobin (oxyHb) (n ＝ 12). Sodium nitroprusside was used for comparison. Each of the agents was added in ascending concentration. Relaxation caused by FK409 and FR144420 was significantly greater (p º 0.05) than that by sodium nitroprusside. Relaxation effects of FK409 and FR144420 on the KCl-induced steady contraction were better than those on the oxyHb-induced contraction. FK409 and FR144420 have potential uses for the treatment and prevention of SAH-induced cerebral vasospasm.

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Delayed postoperative neurological deterioration from prolonged sodium nitroprusside administration

Cited by 16 publications

References 12 publications

Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Dysfunction of nitric oxide synthases as a cause and therapeutic target in delayed cerebral vasospasm after SAH

Neurotrophin Protection Against Toxicity Induced by Low Potassium and Nitroprusside in Cultured Cerebellar Granule Neurons

In Vitro Effects of New Generation Fungal Derived Nitric Oxide Donors on Rabbit Basilar Artery

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