Cerebral vasospasm and corticospinal tract injury induced by a modified rat model of subarachnoid hemorrhage

Yang, Qin; J, Gu; Li, Gai‐Li; Xu, Xianhua; Yu, Ke

doi:10.1016/j.jns.2015.08.1536

Cited by 12 publications

(7 citation statements)

References 40 publications

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“…Minimally invasive surgery can evacuate the hematoma with very little injury. The hematoma and the intracranial pressure can be efficently removed and reduced when the surgery is assisted with hematoma dissolving drugs [11][12][13]. Urokinase is a hematoma dissolving drug the most widely used with a certain fibrinolytic system effect.…”

Section: Discussionmentioning

confidence: 99%

Curative effect of minimally invasive puncture and drainage assisted with alteplase on treatment of acute intracerebral hemorrhage

Zhang

2016

JAD

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Section: Discussionmentioning

confidence: 99%

Curative effect of minimally invasive puncture and drainage assisted with alteplase on treatment of acute intracerebral hemorrhage

Zhang

2016

JAD

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“…Seven days before testing, the rats were deeply intraperitoneally anesthetized with a combination of medetomidine/midazolam/butorphanol anesthesia (0.15/2.0/5.0 mg/kg, respectively). The anesthetic conditions were continuously verified through the experiment (maintained during electrode implantation, SAH induction and during data recording 7 days after) in all animals (Fujiki et al, 2004(Fujiki et al, , 2020aQin et al, 2015;Mishra et al, 2017). Briefly, the absence of pedal withdrawal (''toe-pinch'') reflex was used for assessment of anesthesia and analgesia depth, and the body temperature was maintained at 37 • C intra-and postoperatively with a temperature-controlled heating pad.…”

Section: Induction Of Cisterna Magna Sah Modelmentioning

confidence: 99%

Blockade of Motor Cortical Long-Term Potentiation Induction by Glutamatergic Dysfunction Causes Abnormal Neurobehavior in an Experimental Subarachnoid Hemorrhage Model

Fujiki

Kuga

Ozaki

et al. 2021

Front. Neural Circuits

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Subarachnoid hemorrhage (SAH) is a life-threatening condition that can also lead to permanent paralysis. However, the mechanisms that underlying neurobehavioral deficits after SAH have not been fully elucidated. As theta burst stimulation (TBS) can induce long-term potentiation (LTP) in the motor cortex, we tested its potential as a functional evaluation tool after experimentally induced SAH. Motor cortical inter-neuronal excitability was evaluated in anesthetized rats after 200 Hz-quadripulse TBS (QTS5), 200 Hz-quadripulse stimulation (QPS5), and 400 Hz-octapulse stimulation (OPS2.5). Furthermore, correlation between motor cortical LTP and N-methyl-D-aspartate-receptor activation was evaluated using MK-801, a NMDA-receptor antagonist. We evaluated inhibition-facilitation configurations [interstimulus interval: 3 ms; short-latency intracortical inhibition (SICI) and 11 ms; intracortical facilitation (ICF)] with paired electrical stimulation protocols and the effect of TBS paradigm on continuous recording of motor-evoked potentials (MEPs) for quantitative parameters. SAH and MK-801 completely blocked ICF, while SICI was preserved. QTS5, QPS5, and OPS2.5 facilitated continuous MEPs, persisting for 180 min. Both SAH and MK-801 completely blocked MEP facilitations after QPS5 and OPS2.5, while MEP facilitations after QTS5 were preserved. Significant correlations were found among neurological scores and 3 ms-SICI rates, 11 ms-ICF rates, and MEP facilitation rates after 200 Hz-QTS5, 7 days after SAH (R2 = 0.6236; r = −0.79, R2 = 0.6053; r = −0.77 and R2 = 0.9071; r = 0.95, p < 0.05, respectively). Although these findings need to be verified in humans, our study demonstrates that the neurophysiological parameters 3 ms-SICI, 11 ms-ICF, and 200 Hz-QTS5-MEPs may be useful surrogate quantitative biomarkers for assessing inter-neuronal function after SAH.

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“…Subarachnoid hemorrhage (SAH) has a high morbidity and mortality worldwide . About two‐thirds of SAH patients develop cerebral vasospasm (CVS) within 3‐14 days which could increase the risk of delayed cerebral ischemia (DCI) . About 50% of patients with vasospasm develop DCI, but the relationship between them has been questioned .…”

Section: Introductionmentioning

confidence: 99%

“…1 About two-thirds of SAH patients develop cerebral vasospasm (CVS) within 3-14 days 2 which could increase the risk of delayed cerebral ischemia (DCI). 3 About 50% of patients with vasospasm develop DCI, but the relationship between them has been questioned. 2 Meanwhile, CVS and DCI were the major causes of disability and death after SAH.…”

Section: Introductionmentioning

confidence: 99%

Salvinorin A ameliorates cerebral vasospasm through activation of endothelial nitric oxide synthase in a rat model of subarachnoid hemorrhage

Sun

Zhang

et al. 2018

Microcirculation

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Cerebral vasospasm and corticospinal tract injury induced by a modified rat model of subarachnoid hemorrhage

Cited by 12 publications

References 40 publications

Curative effect of minimally invasive puncture and drainage assisted with alteplase on treatment of acute intracerebral hemorrhage

Curative effect of minimally invasive puncture and drainage assisted with alteplase on treatment of acute intracerebral hemorrhage

Blockade of Motor Cortical Long-Term Potentiation Induction by Glutamatergic Dysfunction Causes Abnormal Neurobehavior in an Experimental Subarachnoid Hemorrhage Model

Salvinorin A ameliorates cerebral vasospasm through activation of endothelial nitric oxide synthase in a rat model of subarachnoid hemorrhage

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