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1 opment of an effective therapy to ameliorate cerebral vasospasm.
2 approach for the prevention and treatment of cerebral vasospasm.
3 currence and severity of sequelae, including cerebral vasospasm.
4 much has been written about the treatment of cerebral vasospasm.
5 plicated by pathological vasoconstriction or cerebral vasospasm.
6 ic oxide synthase, have been used to prevent cerebral vasospasm after aneurysmal subarachnoid hemorrh
7 hether recombinant OPN (r-OPN) could prevent cerebral vasospasm after subarachnoid hemorrhage (SAH) i
8 , including increased intracranial pressure, cerebral vasospasm and ischemia, glutamate excitotoxicit
9 iovascular variables, detecting and treating cerebral vasospasm and managing systemic complications.
10 acid peptide that has been closely linked to cerebral vasospasm and more recently to oxidative stress
11 in into the CSF inhibited hemoglobin-induced cerebral vasospasm and preserved vascular NO signaling.
12 , emphasizing the detection and treatment of cerebral vasospasm and the management of systemic compli
13 orts regarding hyperthermia, cerebral edema, cerebral vasospasm, and lethal interactions with commonl
14 95 fasudil was approved for the treatment of cerebral vasospasm, and more recently, ripasudil was app
15 n (oxyhb) has been implicated in SAH-induced cerebral vasospasm as it causes cerebral artery constric
16 ng sequential brain imaging and investigated cerebral vasospasm by angiography or time-of-flight magn
17 ns in normal cerebral blood flow, such as in cerebral vasospasm, can induce neurological deficits.
18 Besides classical contributors like proximal cerebral vasospasm, CSD clusters may reduce O(2) supply
19                                              Cerebral vasospasm (CV) and the resulting delayed cerebr
20 observation, blood pressure (BP) management, cerebral vasospasm (CV) prophylaxis and the need for dig
21 cted in the role of intestinal microbiome in cerebral vasospasm (CVS) after aneurysmal subarachnoid h
22                                              Cerebral vasospasm (CVS) is an important contributor to
23 rotective in animal models and may attenuate cerebral vasospasm (cVSP) in human aneurysmal subarachno
24   Diabetics have a higher risk of developing cerebral vasospasms (CVSP) after subarachnoid hemorrhagi
25                             Brain injury and cerebral vasospasm during the 14 days after the subarach
26                                              Cerebral vasospasm following aneurysmal subarachnoid hem
27                                              Cerebral vasospasm has traditionally been regarded as an
28 oppler has an established role in diagnosing cerebral vasospasm in patients with aneurysmal subarachn
29 mortality, and the occurrence of symptomatic cerebral vasospasm in patients with aneurysmal subarachn
30 ch that potentiates vascular remodeling, and cerebral vasospasm, in bTBI patients.
31                                              Cerebral vasospasm is a dreaded sequelae of aneurysmal s
32                                              Cerebral vasospasm is a frequent complication after suba
33                                              Cerebral vasospasm is a recognised but poorly understood
34  endothelin-1 (ET-1) is induced resulting in cerebral vasospasm, ischemia, reperfusion and the activa
35                                              Cerebral vasospasm largely contributes to a devastating
36                                              Cerebral vasospasm occurs more frequently, and with earl
37 ation of cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice.
38 ructures in the cerebrospinal fluid (CSF) of cerebral vasospasm patients has been made.
39 ia ink-gelatin casting for the assessment of cerebral vasospasm, permits outstanding immunohistochemi
40 es that depict the onset of the accompanying cerebral vasospasm, preventive and therapeutic options a
41 o consensus on inpatient treatment including cerebral vasospasm prophylaxis and follow-up imaging for
42                 In case 1 and case 2 neither cerebral vasospasm prophylaxis nor transcranial doppler
43 l, a ROCK inhibitor used clinically to treat cerebral vasospasm, restored platelet counts in adult mi
44                     In aSAH individuals with cerebral vasospasm, sustained increase of blood pressure
45 impending cerebral ischemia in patients with cerebral vasospasm.Trial registration number: German cli
46 we developed a novel technique for assessing cerebral vasospasm using cerebrovascular perfusion with
47                                              Cerebral vasospasm (VSP) is a common phenomenon after an
48                   In the overall population, cerebral vasospasm was significantly less common in the
49 thromboxane A2 implicated in the etiology of cerebral vasospasm, we observed significant increases in