scholarly journals Serum Sodium Concentration Changes Causes Delayed Cerebral Vasospasm in Patients with Aneurysmal Subarachnoid Hemorrhage.

2000 ◽  
Vol 11 (2) ◽  
pp. 52-60
Author(s):  
Yasumitsu Mizobata ◽  
Junichiro Yokota ◽  
Hideho Ryujin ◽  
Ken Takahara ◽  
Yoshikazu Nakajima
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Serum Sodium ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Delayed Cerebral Vasospasm ◽  
Concentration Changes

Serum Sodium Concentration Changes Are Related to Fluid Balance and Sweat Sodium Loss

2010 ◽  
Vol 42 (9) ◽  
pp. 1669-1674 ◽  
Author(s):  
MATTHEW D. PAHNKE ◽  
JOEL D. TRINITY ◽  
JEFFREY J. ZACHWIEJA ◽  
JOHN R. STOFAN ◽  
W. DOUGLAS HILLER ◽  
...  
Keyword(s):  
Fluid Balance ◽  
Serum Sodium ◽  
Sodium Concentration ◽  
Serum Sodium Concentration ◽  
Concentration Changes ◽  
Sodium Loss ◽  
Sweat Sodium

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

scholarly journals Matrix Metalloproteinases in Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
Vivek Mehta ◽  
Jonathan Russin ◽  
Alexandra Spirtos ◽  
Shuhan He ◽  
Peter Adamczyk ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Matrix Metalloproteinases ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Critical Role ◽  
Morbidity And Mortality ◽  
Cellular Mechanisms ◽  
Delayed Cerebral Vasospasm ◽  
Membrane Bound ◽  
Existing Data

Delayed cerebral vasospasm is a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). While the cellular mechanisms underlying vasospasm remain unclear, it is believed that inflammation may play a critical role in vasospasm. Matrix metalloproteinasees (MMPs) are a family of extracellular and membrane-bound proteases capable of degrading the blood-rain barrier (BBB). As such, MMP upregulation following SAH may result in a proinflammatory extravascular environment capable of inciting delayed cerebral vasospasm. This paper presents an overview of MMPs and describes existing data pertinent to delayed cerebral vasospasm.

Simvastatin for the Prevention of Delayed Cerebral Vasospasm and Delayed Cerebral Ischemia Following Aneurysmal Subarachnoid Hemorrhage

US Neurology ◽  
2010 ◽  
Vol 05 (02) ◽  
pp. 58
Author(s):  
Kassi Kronfeld ◽  
Sherry Hsiang-Yi Chou ◽  
◽  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Animal Studies ◽  
Randomized Clinical Trials ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Delayed Cerebral Ischemia ◽  
Delayed Cerebral Vasospasm ◽  
Life Years ◽  
The Us

Aneurysmal subarachnoid hemorrhage (SAH) affects over 30,000 people annually in the US and is responsible for 27% of all stroke-related potential life-years lost before 65 years of age. Delayed cerebral vasospasm, defined as the narrowing of the cerebral arteries at the base of the brain, can occur several days after the initial SAH and cause significant additional morbidity and mortality. Currently, preventive and therapeutic options for delayed cerebral vasospasm are limited and may involve high risk. Oral nimodipine is the only therapeutic agent proven to modestly improve outcome following SAH in multicenter randomized clinical trials. Statins have pleiotropic effects targeting many known pathways in cerebral vasospasm pathogenesis and show promise as potential new therapeutic agents for delayed vasospasm in preliminary animal studies, while results from human data are mixed. In this article, we review the known pathogenic mechanisms of delayed cerebral vasospasm, pre-clinical animal studies on statin use and delayed cerebral vasospasm, and results from human studies to date.

Association of an endogenous inhibitor of nitric oxide synthase with cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

2007 ◽  
Vol 107 (5) ◽  
pp. 945-950 ◽  
Author(s):  
Carla S. Jung ◽  
Edward H. Oldfield ◽  
Judith Harvey-White ◽  
Michael G. Espey ◽  
Michael Zimmermann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Type I ◽  
Endogenous Inhibitor ◽  
Primate Model ◽  
Delayed Cerebral Vasospasm

Object Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) may be evoked by the decreased availability of nitric oxide (NO). Increased cerebrospinal fluid (CSF) levels of asymmetric dimethyl-l-arginine (ADMA), an endogenous inhibitor of NO synthase (NOS), have been associated with the course and degree of cerebral vasospasm in a primate model of SAH. In this study, the authors sought to determine if similar changes in CSF ADMA levels are observed in patients with SAH, and whether these changes are associated with NO and NOS metabolite levels in the CSF and the presence of cerebral vasospasm. Methods Asymmetric dimethyl-l-arginine, l-arginine, l-citrulline, and nitrite levels were measured in CSF and serum samples collected during the 21-day period after a single aneurysmal SAH in 18 consecutive patients. Samples were also obtained in a control group consisting of seven patients with Chiari malformation Type I and five patients with spontaneous intracerebral hemorrhage without SAH. Vasospasm, defined as a greater than 11% reduction in the anterior circulation vessel diameter ratio compared with the ratio calculated from the initial arteriogram, was assessed on cerebral arteriography performed around Day 7. Results In 13 patients with SAH, arteriographic cerebral vasospasm developed. Cerebrospinal fluid ADMA levels in patients with SAH were higher than in those in the control group (p < 0.001). The CSF ADMA level remained unchanged in the five patients with SAH without vasospasm, but was significantly increased in patients with vasospasm after Day 3 (6.2 ± 1.7 μM) peaking during Days 7 through 9 (13.3 ± 6.7 μM; p < 0.001) and then gradually decreasing between Days 12 and 21 (8.8 ± 3.2 μM; p < 0.05). Nitrite levels in the CSF were lower in patients with vasospasm compared to patients without vasospasm (p < 0.03). Cerebrospinal fluid ADMA levels positively correlated with the degree of vasospasm (correlation coefficient [CC] = 0.88, p = 0.0001; 95% confidence interval [CI] 0.74–0.95) and negatively correlated with CSF nitrite levels (CC = −0.55; p = 0.017; 95% CI −0.81 to −0.12). Conclusions These results support the hypothesis that ADMA is involved in the progression of cerebral vasospasm. Asymmetric dimethyl-l-arginine and its metabolizing enzymes may be a future target for treatment of cerebral vasospasm after SAH.

scholarly journals Molecular biological considerations in cerebral vasospasm following aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 3 (3) ◽  
pp. E5 ◽  
Author(s):  
Jeffrey E. Thomas
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
No Production ◽  
Vasoactive Substances ◽  
Delayed Cerebral Vasospasm ◽  
Enhanced Production ◽  
A Cell ◽  
Vasoconstrictor Peptide

Chronic delayed cerebral vasospasm (CDCV) remains a serious and often fatal complication of aneurysmal subarachnoid hemorrhage (SAH). The current understanding of its fundamental mechanisms and molecular biological characterization is rudimentary. Two important vasoactive substances have been implicated in CDCV: endothelin-1 (ET-1) and nitric oxide (NO). A 21-amino acid vasoconstrictor peptide, ET-1 has generated interest as a possible important contributor to cerebral vasospasm on the basis of both clinical and experimental evidence suggesting abnormally enhanced production. Nitric oxide is a cell membrane-permeable free radical gas that accounts for the vasodilatory effect of endothelium-derived relaxation factor and is a physiological antagonist of ET-1. As with ET-1, abnormalities of NO production have been implicated in several pathological conditions including cerebral vasospasm. This brief report reviews some of the physiological and regulatory features of these two molecules and explores the possibility of their relationship to cerebral vasospasm.

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