Dysfunction of nitric oxide in the spastic basilar arteries after subarachnoid hemorrhage

Suzuki, Yoshio; Kajita, Yasukazu; Oyama, Hirofumi; Tanazawa, Toshihiko; Takayasu, Misako; Shibuya, Masabumi; Sugita, Kenichiro

doi:10.1016/0165-1838(94)90093-0

Cited by 18 publications

(11 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This decrease in NO availability in the arterial wall is a putative cause of vasospasm. 8,45,51,56 Supporting this hypothesis are the reduced levels of cGMP, the second messenger for biological activity of NO, 19 in the wall of cerebral arteries exposed to blood 8,23,25 and the reversal 1 and prevention of vasospasm after an intracarotid infusion of NO. 44 In the primate model of SAH, vasospasm resolves approximately 14 days after onset of SAH.…”

Section: Discussionmentioning

confidence: 83%

See 1 more Smart Citation

Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage

Pluta¹,

Afshar²,

Thompson³

et al. 2000

Journal of Neurosurgery

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 83%

“…4,11,14,16,34,48,57 Subsequently, L-arginine has been proposed as a potential therapy for delayed cerebral vasospasm. 13,22,51,53 We sought to establish whether intracarotid or intravenous infusion of L-arginine reverses or prevents vasospasm in a primate model of SAH.…”

Section: Discussionmentioning

confidence: 99%

Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage

Pluta¹,

Afshar²,

Thompson³

et al. 2000

Journal of Neurosurgery

View full text Add to dashboard Cite

show abstract

“…These include scavenging by hemoglobin, changes in the amount or activity of NOS, and depletion of substrate or cofactors. Previous studies have reported that NOS enzymatic activity is (13) or is not (22,42) changed after SAH. In the present study, we found no change in Michaelis-Menten V max and K m , indicating that NOS was not irreversibly inactivated or altered in its kinetics during the first phase of acute NO depletion.…”

Section: Discussionmentioning

confidence: 97%

Nitric Oxide Synthase in Acute Alteration of Nitric Oxide Levels after Subarachnoid Hemorrhage

et al. 2004

View full text Add to dashboard Cite

show abstract

“…45,46 Involvement of NO has been implicated in SAH. 6,21,47,48 Several investigators have shown that production of cGMP in vascular smooth muscle is decreased following SAH. 16,17 However, since NO donors can still produce relaxation of these blood vessels, 49 decreased vasodilatation may be due to reduction in basal cerebral NO levels.…”

Section: Discussionmentioning

confidence: 99%

“…46,50,51 Because SAH does not affect the ability of cerebral arteries to synthesize NO. 46,47,52 decreased NO may occur as the result of scaveng- ing by hemoglobin, or free radicals. 46,48,51 If decreased availability of NO leads to vasoconstriction, administering an NO donor could potentially reverse this effect.…”

Section: Discussionmentioning

confidence: 99%

Effects of S -Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage

Sehba

Ding

Chereshnev

et al. 1999

Stroke

101

View full text Add to dashboard Cite

Background and Purpose-Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH. Methods-SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 mol/L/kg, nϭ31) or saline (nϭ21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 mol/L/kg, nϭ5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically. Results-GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6Ϯ26.6% versus saline 37. Key Words: cerebral blood flow Ⅲ glutamates Ⅲ nitric oxide Ⅲ subarachnoid hemorrhage Ⅲ vasoconstriction C erebral arteries respond to subarachnoid hemorrhage (SAH) with a biphasic contraction that begins minutes after the bleed and delayed vasospasm more than 48 hours later. 1-3 Although a great deal is known about the mechanisms and management of delayed vasospasm, less is known about the physiology, treatment, and importance of acute vasoconstriction. Different mechanisms may underlie the 2 processes, 4 and a great variety have been implicated. [5][6][7][8][9][10][11] Recently we have shown that acute vasoconstriction is associated with decreased cerebral blood flow (CBF), ischemic glutamate release, and premature mortality after experimental SAH. 12 If acute vasoconstriction could be pharmacologically attenuated, then SAH-induced brain injury could potentially be reduced.Resting cerebrovascular tone is maintained by a balance between opposing vasoconstrictive and vasodilatory forces, and both are pathologically altered in the acute phases of SAH. One of the most important of these is the resting vasodilatory influence of nitric oxide (NO). NO has been shown to induce endothelium-dependent vasodilatation via a cGMP-mediated See Editorial Comment, page 1961 mechanism. 13 Loss of endothelium-mediated vasodilatation 14,15 and decreased cGMP production 16,17 have been shown to contribute to vasospasm after SAH.Because administration of an NO donor after SAH should potentially restore c-GMP-dependent vasodilatation, a number of different NO donors have been tested for their ability to attenuate delayed vasospasm. 18 -21 Recent studies have suggested that sodium nitroprusside administered intrathecally 22 or intra-arterially 23 increases CBF acutely after SAH. In preliminary studies we have found that it also causes profound hypotension in this setting (J.B. Bederson, MD, et al, ...

show abstract

Dysfunction of nitric oxide in the spastic basilar arteries after subarachnoid hemorrhage

Cited by 18 publications

References 7 publications

Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage

Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage

Nitric Oxide Synthase in Acute Alteration of Nitric Oxide Levels after Subarachnoid Hemorrhage

Effects of S -Nitrosoglutathione on Acute Vasoconstriction and Glutamate Release After Subarachnoid Hemorrhage

Contact Info

Product

Resources

About