Acute Vasoconstriction after Subarachnoid Hemorrhage

Bederson, Joshua B.; Levy, A; Ding, Wan Hong; Kahn, Ronald A.; DiPerna, Costanzo A.; Jenkins, Arthur L.; Vallabhajosyula, Prashanth

doi:10.1097/00006123-199802000-00091

Cited by 272 publications

(246 citation statements)

References 67 publications

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“…However, it did not recover completely, and a relevant hypoperfusion persisted even hours after CPP had returned to near normal values. This observation most likely resembles the phenomenon of acute vasoconstriction after SAH (Bederson et al, 1998). Its persistence may constitute a reduced basis of CBF, which might be amplified by other factors.…”

Section: Cerebral Blood Flow and Acute Vasoconstrictionmentioning

confidence: 59%

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

Westermaier

Jauss

Eriskat

et al. 2009

J Cereb Blood Flow Metab

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Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO 2 ) in the first 6 h after experimental SAH. Sixteen Sprague-Dawley rats were subjected to SAH using the endovascular filament model or served as controls (n = 8). Bilateral local cortical blood flow, intracranial pressure, cerebral perfusion pressure, and ptiO 2 were followed for 6 h after SAH. After induction of SAH, local cortical blood flow rapidly declined to 22% of baseline and returned to 80% after 6 h. The decline of local cortical blood flow markedly exceeded the decline of cerebral perfusion pressure. ptiO 2 declined to 57%, recovered after 2 h, and reached Z140% of baseline after 6 h. Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.

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Section: Cerebral Blood Flow and Acute Vasoconstrictionmentioning

confidence: 59%

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

Westermaier

Jauss

Eriskat

et al. 2009

J Cereb Blood Flow Metab

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“…We hypothesize that disturbances in this pathway con tribute to acute vasoconstriction after SAH (Bederson et a!., 1998;Schwartz et a!., 1999;. However, little direct evidence of decreased NO avail ability in the acute phases of SAH has been presented.…”

Section: Discussionmentioning

confidence: 95%

“…Decreased NO levels observed in the current study makes SAH unique among the various forms of ischemic insults (Kader et a!., 1993;Kumura et a!., 1994;Malinski et a!., 1993). An initial decrease in NO availability may con tribute to SAH-induced brain injury by initiating a series of events including unopposed vasoconstriction, de creased CBF, ischemia, and glutamate release (Bederson et a!., 1995;Bederson et a!., 1998;Schwartz et aI., 1999; as well as Ca+ 2 influx, activation of NOS, and subsequently increased NO production.…”

Section: Discussionmentioning

confidence: 99%

“…• SAH (180 min) Subarachnoid hemorrhage induces an acute global ischemic insult (Bederson et a!., 1998), which is the pri mary cause of morbidity and mortality in humans (Bro derick et a!., 1994;Kassell et a!., 1985). We previously demonstrated that acute cerebral vasoconstriction con tributes to this ischemia (Bederson et aI., 1998) and that decreased NO availability plays important role in this process (Schwartz et a!., 1999;.…”

mentioning

confidence: 99%

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Acute Decrease in Cerebral Nitric Oxide Levels after Subarachnoid Hemorrhage

Sehba

Schwartz

Chereshnev

et al. 2000

J Cereb Blood Flow Metab

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132

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Summary: Disturbances in the nitric oxide (NO) vasodilatory pathway have been implicated in acute vasoconstriction and ischemia after subarachnoid hemorrhage (SAH). The authors hypothesize that blood released during SAH leads to vasocon striction by scavenging NO and limiting its availability. This was tested by measuring the major NO metabolites nitrite and nitrate in five different brain regions before and after experi mental SAH. The basal NO metabolites levels were as follows (mean ± SO, f.Lmol/mg wet weight): brain stem, 0.14 ± 0.07; cerebellum, 0.12 ± 0.08; ventral convexity cortex, 0.22 ± 0.15; dorsal convexity cortex, 0.16 ± 0.11; and hippocampus, 0.26 ± 0.17. In sham-operated animals, no effect of the nitric oxide synthase (NOS) inhibitor L G -nitro-L-arginine-methyl-ester (30 mg/kg) was found on NO metabolites 40 minutes after admin istration, but a significant decrease was seen after 120 minutes.Cerebral blood flow decreases acutely and ischemic injury occurs after subarachnoid hemorrhage (SAH) in both experimental and clinical studies. Cerebral arteries have been shown to respond to SAH with a biphasic constriction. An acute constriction begins minutes after the bleed, and delayed vasospasm begins 48 hours later . Although the significance of de layed vasospasm is recognized (Sobey and Faraci, 1998 604The NO metabolites decreased significantly 10 minutes after SAH in all brain regions except for hippocampus, and recov ered to control levels in cerebellum at 60 minutes and in brain stem and dorsal cerebral cortex 180 minutes after SAH, while remaining low in ventral convexity cortex. Nitrite recovered completely in all brain regions at 180 minutes after SAH, whereas nitrate remained decreased in brain stem and ventral convexity cortex. Our results indicate that SAH causes acute decreases in cerebral NO levels by a mechanism other than NOS inhibition and provide further support for the hypothesis that alterations in the NO vasodilatory pathway contribute di rectly to the ischemic insult after SAH.

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“…58,[66][67][68] Acute hypoperfusions are attributed to reversible microvasoconstriction in a rat model of mTBI, 69 and acute vasoconstriction has been reported within an hour after TBI in human survivors with subarachnoid hemorrhage. 70,71 Further, even transient hypoperfusion may produce prolonged changes in cortical thickness as evidenced by decreased cortical thickness and less fMRI activation in rats at 4 months after a single episode of hypoxia-ischemia. 72 Future studies that simultaneously measure cortical thickness and perfusion at an early stage after mTBI may shed light on this relationship.…”

Section: Early Cortical Thinning In Mtbi Survivors After Mvcsmentioning

confidence: 99%

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

Wang

Xie

Cotton

et al. 2015

Journal of Neurotrauma

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In a motor vehicle collision (MVC), survivors often receive mild traumatic brain injuries (mTBI). Although there have been some reports of early white matter changes after an mTBI, much less is known about early cortical structural changes. To investigate early cortical changes within a few days after an MVC, we compared cortical thickness of mTBI survivors with nonmTBI survivors, then reexamined cortical thickness in the same survivors 3 months later. MVC survivors were categorized as mTBI or non-mTBI based on concussive symptoms documented in emergency departments (EDs). Cortical thickness was measured from MRI images using FreeSurfer within a few days and again at 3 months after MVC. Post-traumatic stress symptoms and physical conditions were also assessed. Compared with the non-mTBI group (n = 23), the mTBI group (n = 21) had thicker cortex in the left rostral middle frontal (rMFG) and right precuneus gyri, but thinner cortex in the left posterior middle temporal gyrus at 7.2 -3.1 days after MVC. After 3 months, cortical thickness had decreased in left rMFG in the mTBI group but not in the non-mTBI group. The cortical thickness of the right precuneus region in the initial scans was positively correlated with acute traumatic stress symptoms for all survivors and with the number of reduced activity days for mTBI survivors who completed the follow-up. The preliminary results suggest that alterations in cortical thickness may occur at an early stage of mTBI and that frontal cortex structure may change dynamically over the initial 3 months after mTBI.

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Acute Vasoconstriction after Subarachnoid Hemorrhage

Cited by 272 publications

References 67 publications

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

Acute Decrease in Cerebral Nitric Oxide Levels after Subarachnoid Hemorrhage

Early Cortical Thickness Change after Mild Traumatic Brain Injury following Motor Vehicle Collision

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