scholarly journals Vasospasm as the sole cause of cerebral ischemia: how strong is the evidence?

2006 ◽  
Vol 21 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Sherman C. Stein ◽  
Joshua M. Levine ◽  
Seema Nagpal ◽  
Peter D. LeRoux
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Potential Role ◽  
Review Literature ◽  
Neurological Deficits ◽  
Therapeutic Approaches ◽  
Large Arteries ◽  
Novel Therapeutic

✓ The authors review literature that challenges the view that vasospasm involving large arteries is the exclusive cause of delayed ischemic neurological deficits (DINDs) following subarachnoid hemorrhage. They discuss alternative mechanisms and review the evidence supporting a potential role for thromboembolism. They conclude that vasospasm and thromboembolism play interrelated and additive roles in the development of DINDs, and that this interaction provides opportunities for novel therapeutic approaches.

Burden of cerebral hypoperfusion in patients with delayed cerebral ischemia after subarachnoid hemorrhage

2020 ◽  
Vol 132 (6) ◽  
pp. 1872-1879
Author(s):  
Hussain Jafri ◽  
Michael N. Diringer ◽  
Michelle Allen ◽  
Allyson R. Zazulia ◽  
Gregory J. Zipfel ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Delayed Cerebral Ischemia ◽  
Area Under The Curve ◽  
Brain Regions ◽  
Cerebral Hypoperfusion ◽  
Neurological Deficits ◽  
Contralateral Hemisphere ◽  
The Brain ◽  
Abnormal Brain

OBJECTIVEDelayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) may result in focal neurological deficits and cerebral infarction, believed to result from critical regional rather than global impairments in cerebral blood flow (CBF). However, the burden of such regional hypoperfusion has not been evaluated by gold-standard voxel-by-voxel CBF measurements. Specifically, the authors sought to determine whether the proportion of brain affected by hypoperfusion was greater in patients with DCI than in SAH controls without DCI and whether the symptomatic hemisphere (in those with lateralizing deficits) exhibited a greater cerebral hypoperfusion burden.METHODSSixty-one patients with aneurysmal SAH underwent 15O PET to measure regional CBF during the period of risk for DCI (median 8 days after SAH, IQR 7–10 days). Regions of visibly abnormal brain on head CT studies, including areas of hemorrhage and infarction, were excluded. Burden of hypoperfusion was defined as the proportion of PET voxels in normal-appearing brain with CBF < 25 ml/100 g/min. Global CBF and hypoperfusion burden were compared between patients with and those without DCI at the time of PET. For patients with focal impairments from DCI, the authors also compared average CBF and hypoperfusion burden in symptomatic versus asymptomatic hemispheres.RESULTSTwenty-three patients (38%) had clinical DCI at the time of PET. Those with DCI had higher mean arterial pressure (MAP; 126 ± 14 vs 106 ± 12 mm Hg, p < 0.001) and 18 (78%) were on vasopressor therapy at the time of PET study. While global CBF was not significantly lower in patients with DCI (mean 39.4 ± 11.2 vs 43.0 ± 8.3 ml/100 g/min, p = 0.16), the burden of hypoperfusion was greater (20%, IQR 12%–23%, vs 12%, 9%–16%, p = 0.006). Burden of hypoperfusion performed better than global CBF as a predictor of DCI (area under the curve 0.71 vs 0.65, p = 0.044). Neither global CBF nor hypoperfusion burden differed in patients who responded to therapy compared to those who had not improved by the time of PET. Although hemispheric CBF was not lower in the symptomatic versus contralateral hemisphere in the 13 patients with focal deficits, there was a trend toward greater burden of hypoperfusion in the symptomatic hemisphere (21% vs 18%, p = 0.049).CONCLUSIONSThe burden of hypoperfusion was greater in patients with DCI, despite hemodynamic therapies, higher MAP, and equivalent global CBF. Similarly, hypoperfusion burden was greater in the symptomatic hemisphere of DCI patients with focal deficits even though the average CBF was similar to that in the contralateral hemisphere. Evaluating the proportion of the brain with critical hypoperfusion after SAH may better capture the extent of DCI than averaging CBF across heterogenous brain regions.

scholarly journals Vasospasm and delayed cerebral ischemia after uneventful clipping of an unruptured intracranial aneurysm – a case report

BMC Neurology ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Christin Campe ◽  
Jens Neumann ◽  
I. Erol Sandalcioglu ◽  
Ali Rashidi ◽  
Michael Luchtmann
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Motor Speech Disorder ◽  
Unruptured Intracranial Aneurysms ◽  
Short Period ◽  
The Right

Abstract Background Due to improvements in both the quality and availability of intracranial imaging as well as the evolution of surgical and endovascular techniques during the last decade, the number of treatments of unruptured intracranial aneurysms (UIA) has increased steadily. However, it is not generally known that vasospasm can arise after an uneventful clipping. Case presentation We present a case of a 69-year-old woman who suffered from vasospasm and delayed cerebral ischemia that occurred after an uneventful clipping of a UIA. The aneurysm of the right middle cerebral artery was found incidentally via magnetic resonance imaging ordered after the patient complained of a short period of slight gait disturbances. To avoid a subarachnoid hemorrhage and consecutive complications like vasospasms, the patient elected microsurgical treatment. Clipping was managed by keyhole approach. Temporal clipping of the M1 was not necessary. After clip placement, appropriate flow in all distal segments was confirmed by indocyanine green video-angiography and micro-Doppler. The patient was discharged seven days after surgery without neurological deficits. After 12 days, the patient developed at home a sudden drooping on the left side of the face. Upon admission to the emergency room, the patient was alert but slightly confused. Neurological examination revealed a left-sided hemiparesis and motor speech disorder. In contrast to the preoperative transfemoral catheter angiography, the subsequent right internal carotid angiogram showed clear signs of vasospasm along the M1 and M2 segments of the right middle cerebral artery. Antithrombotic treatment with acetylsalicylic acid was begun. In accordance with guidelines for the treatment of subarachnoid hemorrhage and vasospasm, nimodipine was added. After 11 days the patient was discharged with no symptoms. Conclusion Cerebral vasospasm as a cause of ischemic stroke after uneventful surgery for a UIA seems to be a rare but possibly underestimated etiology that demands particular attention with respect to providing appropriate treatment. In future, it may be prudent to perform follow-up transcranial ultrasonography testing after the clipping of a UIA, especially considering the availability of potentially neuroprotective medications like nimodipine.

Short-Term Antifibrinolytic Therapy Before Early Aneurysm Treatment in Subarachnoid Hemorrhage: Effects on Rehemorrhage, Cerebral Ischemia, and Hydrocephalus

Neurosurgery ◽  
2010 ◽  
Vol 67 (4) ◽  
pp. 935-940 ◽  
Author(s):  
Mark R Harrigan ◽  
Kiran F Rajneesh ◽  
Agnieszka A Ardelt ◽  
Winfield S Fisher
Keyword(s):  
Ischemic Stroke ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Aminocaproic Acid ◽  
Neurological Deficits ◽  
Short Term ◽  
Symptomatic Vasospasm ◽  
Term Administration ◽  
Ischemic Complications

Abstract BACKGROUND: Long-term administration of the antifibrinolytic agent epsilon aminocaproic acid (EACA) reduces the rate of rehemorrhage in patients with aneurysmal subarachnoid hemorrhage (SAH), but is associated with cerebral ischemia. OBJECTIVE: To evaluate short-term administration of EACA before early surgery in patients with SAH. METHODS: Retrospective review of 356 patients admitted between June 2002 and December 2007 with a diagnosis of aneurysmal SAH. Medical records were reviewed to determine SAH risk factors, clinical grade at the time of admission, and incidence of rehemorrhage, permanent new-onset focal neurological deficits, computed tomography evidence of cerebral infarction, symptomatic vasospasm, and hydrocephalus. RESULTS: Patients underwent treatment of the ruptured aneurysm an average of 47.4 hours after admission and received an average total dose of 40.6 g of EACA. The mean length of time of administration of EACA was 35.6 hours. There was a total of 5 rehemorrhages, for an overall rebleeding rate of 1.4% and a rate of rehemorrhage per 24-hour period of 0.71%. Overall, the rates of symptomatic vasospasm and permanent neurological deficits attributable to ischemic stroke were 11.5% and 7.2%, respectively, and the incidence of shunt-dependent hydrocephalus was 42.3%. Patients who were treated with coiling had higher rates of symptomatic vasospasm and ischemic complications than patients who had surgery. CONCLUSION: Short-term administration of EACA is associated with rates of rehemorrhage, ischemic stroke, and symptomatic vasospasm that compare favorably with historical controls. The rate of hydrocephalus is relatively high and may be attributable to EACA treatment.

scholarly journals Norepinephrine as a Potential Aggravator of Symptomatic Cerebral Vasospasm: Two Cases and Argument for Milrinone Therapy

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
F. A. Zeiler ◽  
J. Silvaggio ◽  
A. M. Kaufmann ◽  
L. M. Gillman ◽  
M. West
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Neurological Examination ◽  
Potential Role ◽  
Delayed Cerebral Ischemia ◽  
High Dose ◽  
Symptomatic Vasospasm ◽  
Blood Pressures ◽  
Hypertensive Therapy

Background.During hypertensive therapy for post-subarachnoid hemorrhage (SAH) symptomatic vasospasm, norepinephrine is commonly used to reach target blood pressures. Concerns over aggravation of vasospasm with norepinephrine exist.Objective.To describe norepinephrine temporally related deterioration in neurological examination of two post-SAH patients in vasospasm.Methods.We retrospectively reviewed two charts of patients with delayed cerebral ischemia (DCI) post-SAH who deteriorated with norepinephrine infusions.Results.We identified two patients with DCI post-SAH who deteriorated during hypertensive therapy with norepinephrine. The first, a 43-year-old male presented to hospital with DCI, failed MABP directed therapy with rapid deterioration in exam with high dose norepinephrine and MABP of 140–150 mm Hg. His exam improved on continuous milrinone and discontinuation of norepinephrine. The second, a 39-year-old female who developed DCI on postbleed day 8 responded to milrinone therapy upfront. During further deterioration and after angioplasty, norepinephrine was utilized to drive MABP to 130–140 mm Hg. Progressive deterioration in examination occurred after angioplasty as norepinephrine doses escalated. After discontinuation of norepinephrine and continuation of milrinone, function dramatically returned but not to baseline.Conclusions.The potential exists for worsening of DCI post-SAH with hypertensive therapy directed by norepinephrine. A potential role exists for vasodilation and inotropic directed therapy with milrinone in the setting of DCI post-SAH.

scholarly journals Delayed Cerebral Ischemia After Subarachnoid Hemorrhage: Is There a Relevant Experimental Model? A Systematic Review of Preclinical Literature

2021 ◽  
Vol 8 ◽  
Author(s):  
Suzanne Goursaud ◽  
Sara Martinez de Lizarrondo ◽  
François Grolleau ◽  
Audrey Chagnot ◽  
Véronique Agin ◽  
...  
Keyword(s):  
Systematic Review ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Related Complication ◽  
Pubmed Database ◽  
Blood Injection ◽  
Definition Of

Delayed cerebral ischemia (DCI) is one of the main prognosis factors for disability after aneurysmal subarachnoid hemorrhage (SAH). The lack of a consensual definition for DCI had limited investigation and care in human until 2010, when a multidisciplinary research expert group proposed to define DCI as the occurrence of cerebral infarction (identified on imaging or histology) associated with clinical deterioration. We performed a systematic review to assess whether preclinical models of SAH meet this definition, focusing on the combination of noninvasive imaging and neurological deficits. To this aim, we searched in PUBMED database and included all rodent SAH models that considered cerebral ischemia and/or neurological outcome and/or vasospasm. Seventy-eight publications were included. Eight different methods were performed to induce SAH, with blood injection in the cisterna magna being the most widely used (n = 39, 50%). Vasospasm was the most investigated SAH-related complication (n = 52, 67%) compared to cerebral ischemia (n = 30, 38%), which was never investigated with imaging. Neurological deficits were also explored (n = 19, 24%). This systematic review shows that no preclinical SAH model meets the 2010 clinical definition of DCI, highlighting the inconsistencies between preclinical and clinical standards. In order to enhance research and favor translation to humans, pertinent SAH animal models reproducing DCI are urgently needed.

Intracarotid slow bolus injection of nimodipine during angiography for treatment of cerebral vasospasm after SAH

1984 ◽  
Vol 61 (2) ◽  
pp. 231-240 ◽  
Author(s):  
J. Andre Grotenhuis ◽  
Winfried Bettag ◽  
B. J. Othmar Fiebach ◽  
Khosrow Dabir
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Calcium Antagonist ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Bolus Injection ◽  
Neurological Deficits ◽  
Cerebral Vessel ◽  
Content Type ◽  
Venous Infusion ◽  
Fine Print

✓ Nimodipine was given as an intracarotid slow bolus injection in six patients with subarachnoid hemorrhage (SAH) due to rupture of a cerebral aneurysm, with angiographically demonstrated vasospasm. The patients were followed by serial angiograms for demonstration of the effect of nimodipine on vasospasm. After angiography, all patients were treated with a constant venous infusion of this new calcium antagonist. Although the therapeutic regimen was started only a few hours after onset of vasospasm, there was no change in cerebral vessel caliber detectable on angiograms following the intracarotid injection. Three patients died, two patients finally recovered with neurological deficits due to cerebral ischemia, and one patient with asymptomatic vasospasm remained symptom-free. Although nimodipine may act to prevent cerebral vasospasm after SAH, the authors believe that the intracarotid application is not effective after vasospasm has occurred.

Plasma endothelin concentrations after aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 92 (3) ◽  
pp. 390-400 ◽  
Author(s):  
Seppo Juvela
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Healthy Volunteers ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Plasma Concentrations ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Content Type ◽  
History Of ◽  
Fine Print

Object. The pathogenesis of cerebral vasospasm and delayed ischemia after subarachnoid hemorrhage (SAH) seems to be complex. An important mediator of chronic vasospasm may be endothelin (ET), with its powerful and long-lasting vasoconstricting activity. In this study the author investigated the correlation between serial plasma concentrations of ET and ischemic symptoms, angiographically demonstrated evidence of vasospasm, and computerized tomography (CT) findings after aneurysmal SAH.Methods. Endothelin-1 immunoreactivity in plasma was studied in 70 patients with aneurysmal SAH and in 25 healthy volunteers by using a double-antibody sandwich-enzyme immunoassay (immunometric) technique.On the whole, mean plasma ET concentrations in patients with SAH (mean ± standard error of mean, 2.1 ± 0.1 pg/ml) did not differ from those of healthy volunteers (1.9 ± 0.2 pg/ml). Endothelin concentrations were significantly higher (p < 0.05) in patients who experienced delayed cerebral ischemia with fixed neurological deficits compared with those in other patients (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml compared with 2.1 ± 0.2 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml compared with 1.9 ± 0.2 pg/ml). Patients with angiographic evidence of severe vasospasm also had significantly (p < 0.05) elevated ET concentrations (post-SAH Days 0–5, 3.2 ± 0.8 pg/ml; post-SAH Days 6–14, 2.7 ± 0.5 pg/ml) as did those with a cerebral infarction larger than a lacuna on the follow-up CT scan (post-SAH Days 0–5, 3.1 ± 0.8 pg/ml; post-SAH Days 6–14, 2.5 ± 0.4 pg/ml) compared with other patients. Patients in whom angiography revealed diffuse moderate-to-severe vasospasm had significantly (p < 0.05) higher ET levels than other patients within 24 hours before or after angiography (2.6 ± 0.3 compared with 1.9 ± 0.2 pg/ml). In addition, patients with a history of hypertension or cigarette smoking experienced cerebral infarctions significantly more often than other patients, although angiography did not demonstrate severe or diffuse vasospasm more often in these patients than in others.Conclusions. Endothelin concentrations seem to correlate with delayed cerebral ischemia and vasospasm after SAH. The highest levels of ET are predictive of the symptoms of cerebral ischemia and vasospasm, and ET may also worsen ischemia in patients with a history of hypertension. Thus, ET may be an important causal or contributing factor to vasospasm, but its significance in the pathogenesis of vasospasm remains unknown.

Abstract P47: Immediate Clinical Improvement Occurs in Patients With Aneurysmal Subarachnoid Hemorrhage and Delayed Cerebral Ischemia Treated With Hypertension Induction or Inotropics

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Carolina Rouanet ◽  
Natalia Vasconcellos ◽  
Feres Eduardo Chaddad Neto ◽  
Gisele Sampaio Silva
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Clinical Improvement ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Treatment Strategies ◽  
Neurological Deficits ◽  
Focal Neurological Deficit ◽  
Level Of Consciousness ◽  
Main Determinants

Introduction: Delayed cerebral ischemia (DCI) is one of the main determinants of prognosis in aneurysmal subarachnoid hemorrhage (aSAH). Hypertension induction (HI) and inotropics are frequently used strategies to treat DCI. However, little is known about clinical improvement immediately after those therapies. Methods: All patients with aSAH admitted to our hospital from 2016 to 2018 were evaluated. DCI was defined as a new focal neurological deficit or decrease in level of consciousness or the appearance of new infarctions on brain imaging. Patients who developed DCI and received vasopressors or inotropics and were included in the study. They were evaluated before (t0), 45 (t1) and 90 (t2) minutes after therapy initiation using NIHSS scores and Glasgow Coma Scale (GCS). Results: A total of 98 aSAH were evaluated, and 21 of them developed DCI (21.4%). Six patients received both treatment strategies, leading to a total of 27 DCI treatments (norepinephrine =12, milrinone =15). Mean NIHSS score had a significant decrease in t1 and t2 when compared to t0 (17 [95%CI 13-24], 16 [95%CI 11-23], 15 [95%CI 9-22], p<0.001 and p<0.002). The same happened among those treated with IH (t0=18 [95%CI 13-25]; t1=16 [95%CI 11-23], p=0.002; t2=14 [95%CI 9-22], p=0.027) and with milrinone (t0=17 [95%CI 12-24]; t1=15 [95%CI 10-23], p=0.007; t2=14 [95%CI 9-23], p=0.001). Mean GCS had a significant improvement in t1, that was not sustained in t2 (9 [95%CI 8-11], 10 [95%CI 9-12], 10 [95%CI 9-12], p=0.008 and p=0.098). In those treated with HI GCS scores did not change significantly (t0=9 [95%CI 7-11]; t1=10 [95%CI 8-12], p=0.054; t2=10 [95%CI 8-12], p=0.177). Those treated with inotropics significantly improved across time (t0=10 [95%CI 8-12]; t1=11 [95%CI 9-13], p=0.004; t2=11 [95%CI 9-13], p=0.001). Conclusions: DCI treatment with HI or inotropic therapy seems effective in immediately improving neurological deficits in patients with aSAH and DCI.

scholarly journals Sirtuin 1 Mediates Protection Against Delayed Cerebral Ischemia in Subarachnoid Hemorrhage in Response to Hypoxic Postconditioning

2021 ◽  
Author(s):  
Deepti Diwan ◽  
Ananth K. Vellimana ◽  
Diane J. Aum ◽  
Julian Clarke ◽  
James W. Nelson ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Sirtuin 1 ◽  
Neurological Deficits ◽  
Multifactorial Disease ◽  
Time Points ◽  
Hypoxic Postconditioning

Background Many therapies designed to prevent delayed cerebral ischemia (DCI) and improve neurological outcome in aneurysmal subarachnoid hemorrhage (SAH) have failed, likely because of targeting only one element of what has proven to be a multifactorial disease. We previously demonstrated that initiating hypoxic conditioning before SAH (hypoxic preconditioning) provides powerful protection against DCI. Here, we expanded upon these findings to determine whether hypoxic conditioning delivered at clinically relevant time points after SAH (hypoxic postconditioning) provides similarly robust DCI protection. Methods and Results In this study, we found that hypoxic postconditioning (8% O 2 for 2 hours) initiated 3 hours after SAH provides strong protection against cerebral vasospasm, microvessel thrombi, and neurological deficits. By pharmacologic and genetic inhibition of SIRT1 (sirtuin 1) using EX527 and global Sirt1 −/− mice, respectively, we demonstrated that this multifaceted DCI protection is SIRT1 mediated. Moreover, genetic overexpression of SIRT1 using Sirt1‐Tg mice, mimicked the DCI protection afforded by hypoxic postconditioning. Finally, we found that post‐SAH administration of resveratrol attenuated cerebral vasospasm, microvessel thrombi, and neurological deficits, and did so in a SIRT1‐dependent fashion. Conclusions The present study indicates that hypoxic postconditioning provides powerful DCI protection when initiated at clinically relevant time points, and that pharmacologic augmentation of SIRT1 activity after SAH can mimic this beneficial effect. We conclude that conditioning‐based therapies administered after SAH hold translational promise for patients with SAH and warrant further investigation.

Scavenging Free Iron Reduces Arteriolar Microvasospasms After Experimental Subarachnoid Hemorrhage

Stroke ◽  
2021 ◽  
Author(s):  
Hanhan Liu ◽  
Julian Schwarting ◽  
Nicole Angela Terpolilli ◽  
Kathrin Nehrkorn ◽  
Nikolaus Plesnila
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Delayed Cerebral Ischemia ◽  
Neurological Deficits ◽  
Free Iron ◽  
Acute Cerebral Ischemia ◽  
Experimental Subarachnoid Hemorrhage ◽  
Underlying Mechanisms ◽  
Novel Therapeutic Strategies

Background and Purpose: Subarachnoid hemorrhage (SAH) is associated with acute and delayed cerebral ischemia resulting in high acute mortality and severe chronic neurological deficits. Spasms of the pial and intraparenchymal microcirculation (microvasospasms) contribute to acute cerebral ischemia after SAH; however, the underlying mechanisms remain unknown. We hypothesize that free iron (Fe 3+ ) released from hemolytic red blood cells into the subarachnoid space may be involved in microvasospasms formation. Methods: Male C57BL/6 mice (n=8/group) received 200 mg/kg of the iron scavenger deferoxamine or vehicle intravenously and were then subjected to SAH by filament perforation. Microvasospasms of pial and intraparenchymal vessels were imaged three hours after SAH by in vivo 2-photon microscopy. Results: Microvasospasms occurred in all investigated vessel categories down to the capillary level. Deferoxamine significantly reduced the number of microvasospasms after experimental SAH. The effect was almost exclusively observed in larger pial arterioles (>30 µm) covered with blood. Conclusions: These results provide proof-of-principle evidence that Fe 3+ is involved in the formation of arteriolar microvasospasms after SAH and that arteriolar and capillary microvasospasms are triggered by different mechanisms. Deciphering the mechanisms of Fe 3+ -induced microvasospasms may result in novel therapeutic strategies for SAH patients.

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