Cerebral vasoconstriction after subarachnoid hemorrhage - Role of changes in vascular receptor phenotype

10.2741/2831 ◽  
2008 ◽  
Vol 13 (13) ◽  
pp. 2160 ◽  
Author(s):  
Jacob Hansen-Schwartz
2006 ◽  
Vol 290 (1) ◽  
pp. R84-R89 ◽  
Author(s):  
Kazuhiko Takeuchi ◽  
Noriyuki Miyata ◽  
Marija Renic ◽  
David R. Harder ◽  
Richard J. Roman

Recent studies have indicated that 20-hydroxyeicosatetraenoic acid (20-HETE) contributes to the fall in cerebral blood flow (CBF) after subarachnoid hemorrhage (SAH), but the factors that stimulate the production of 20-HETE are unknown. This study examines the role of vasoactive factors released by clotting blood vs. the scavenging of nitric oxide (NO) by hemoglobin (Hb) in the fall in CBF after SAH. Intracisternal (icv) injection of blood produced a greater and more prolonged (120 vs. 30 min) decrease in CBF than that produced by a 4% solution of Hb. Pretreating rats with Nω-nitro-l-arginine methyl ester (l-NAME; 10 mg/kg iv) to block the synthesis of NO had no effect on the fall in CBF produced by an icv injection of blood. l-NAME enhanced rather than attenuated the fall in CBF produced by an icv injection of Hb. Blockade of the synthesis of 20-HETE with TS-011 (0.1 mg/kg iv) prevented the sustained fall in CBF produced by an icv injection of blood and the transient vasoconstrictor response to Hb. Hb (0.1%) reduced the diameter of the basilar artery (BA) of rats in vitro by 10 ± 2%. This response was reversed by TS-011 (100 nM). Pretreatment of vessels with l-NAME (300 μM) reduced the diameter of BA and blocked the subsequent vasoconstrictor response to the addition of Hb to the bath. TS-011 returned the diameter of vessels exposed to l-NAME and Hb to that of control. These results suggest that the fall in CBF after SAH is largely due to the release of vasoactive factors by clotting blood rather than the scavenging of NO by Hb and that 20-HETE contributes the vasoconstrictor response of cerebral vessels to both Hb and blood.


2020 ◽  
Vol 10 (3) ◽  
pp. 153 ◽  
Author(s):  
Stefan Wanderer ◽  
Basil E. Grüter ◽  
Fabio Strange ◽  
Sivani Sivanrupan ◽  
Stefano Di Santo ◽  
...  

Background: Delayed cerebral vasospasm (DCVS) due to aneurysmal subarachnoid hemorrhage (aSAH) and its sequela, delayed cerebral ischemia (DCI), are associated with poor functional outcome. Endothelin-1 (ET-1) is known to play a major role in mediating cerebral vasoconstriction. Angiotensin-II-type-1-receptor antagonists such as Sartans may have a beneficial effect after aSAH by reducing DCVS due to crosstalk with the endothelin system. In this review, we discuss the role of Sartans in the treatment of stroke and their potential impact in aSAH. Methods: We conducted a literature research of the MEDLINE PubMed database in accordance with PRISMA criteria on articles published between 1980 to 2019 reviewing: “Sartans AND ischemic stroke”. Of 227 studies, 64 preclinical and 19 clinical trials fulfilled the eligibility criteria. Results: There was a positive effect of Sartans on ischemic stroke in both preclinical and clinical settings (attenuating ischemic brain damage, reducing cerebral inflammation and infarct size, increasing cerebral blood flow). In addition, Sartans reduced DCVS after aSAH in animal models by diminishing the effect of ET-1 mediated vasoconstriction (including cerebral inflammation and cerebral epileptogenic activity reduction, cerebral blood flow autoregulation restoration as well as pressure-dependent cerebral vasoconstriction). Conclusion: Thus, Sartans might play a key role in the treatment of patients with aSAH.


2020 ◽  
pp. 10.1212/CPJ.0000000000000941
Author(s):  
Azam S. Tolla ◽  
Muhammad U. Farooq ◽  
Bradly Haveman-Gould ◽  
Ghassan Naisan ◽  
Philip B. Gorelick

Carotid endarterectomy (CEA) and carotid artery stenting (CAS) are established cerebrovascular procedures to reduce risk of stroke. Complications include stroke, myocardial infarction, and death. A delayed complication following carotid revascularization is cerebral hyperperfusion syndrome (CHS), which can manifest as intracerebral hemorrhage (ICH)[1]. A less common delayed complication of carotid revascularization procedures is reversible cerebral vasoconstriction syndrome (RCVS).


2017 ◽  
Vol 8 ◽  
Author(s):  
Adriano Barreto Nogueira ◽  
Ariel Barreto Nogueira ◽  
José Carlos Esteves Veiga ◽  
Manoel Jacobsen Teixeira

Neurosurgery ◽  
2001 ◽  
Vol 48 (4) ◽  
pp. 854-863
Author(s):  
R. Loch Macdonald ◽  
Bryce K.A. Weir ◽  
Linda S. Marton ◽  
Zhen-Du Zhang ◽  
Michael Sajdak ◽  
...  

2010 ◽  
Vol 152 (12) ◽  
pp. 2167-2172 ◽  
Author(s):  
Ayhan Kanat ◽  
Adem Yilmaz ◽  
Mehmet D. Aydin ◽  
Murat Musluman ◽  
Sare Altas ◽  
...  

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