Time-Dependent Changes in Cerebrospinal Fluid Metal Ions Following Aneurysm Subarachnoid Hemorrhage and Their Association with Cerebral Vasospasm

2014 ◽  
pp. 63-68
Author(s):  
Amit Singla ◽  
Mark R. Villwock ◽  
Margaret A. Riordan ◽  
David J. Padalino ◽  
Eric M. Deshaies
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Metal Ions ◽  
Cerebral Vasospasm ◽  
Time Dependent ◽  
Fluid Metal

Marked reduction of cerebral vasospasm with lumbar drainage of cerebrospinal fluid after subarachnoid hemorrhage

2004 ◽  
Vol 100 (2) ◽  
pp. 215-224 ◽  
Author(s):  
Paul Klimo ◽  
John R. W. Kestle ◽  
Joel D. MacDonald ◽  
Richard H. Schmidt
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Marked Reduction ◽  
Lumbar Drainage

Proteomic Biomarker Discovery in Cerebrospinal Fluid for Cerebral Vasospasm Following Subarachnoid Hemorrhage

2012 ◽  
Vol 21 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Shivanand P. Lad ◽  
Harald Hegen ◽  
Gaurav Gupta ◽  
Florian Deisenhammer ◽  
Gary K. Steinberg
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Biomarker Discovery

Endothelin-1 levels in plasma and cerebrospinal fluid of patients with cerebral vasospasm after aneurysmal subarachnoid hemorrhage

2005 ◽  
Vol 64 ◽  
pp. S2-S5 ◽  
Author(s):  
Iruena Moraes Kessler ◽  
Yolanda Galindo Pacheco ◽  
Silene Paulino Lozzi ◽  
Antônio Santos de Araújo ◽  
Franz Jooji Onishi ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Endothelin 1

scholarly journals Endothelin-1 concentration increases in the cerebrospinal fluid in cerebral vasospasm caused by subarachnoid hemorrhage

2000 ◽  
Vol 53 (2) ◽  
pp. 131-135 ◽  
Author(s):  
Kensuke Suzuki ◽  
Kotoo Meguro ◽  
Takeshi Sakurai ◽  
Yoshifumi Saitoh ◽  
Sadayuki Takeuchi ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Endothelin 1

RELATION BETWEEN CHANGE IN Ca AND Mg LEVELS OF CEREBROSPINAL FLUID AFTER SUBARACHNOID HEMORRHAGE AND THE OCCURRENCE OF VASOSPASM

1998 ◽  
Vol 08 (04) ◽  
pp. 275-282 ◽  
Author(s):  
N. SATO ◽  
K. KURODA ◽  
M. SUZUKI ◽  
A. OGAWA ◽  
K. SERA
Keyword(s):  
Cerebrospinal Fluid ◽  
Trace Elements ◽  
Subarachnoid Hemorrhage ◽  
Muscle Contraction ◽  
Cerebral Vasospasm ◽  
Principal Mechanism ◽  
Cisternal Drainage ◽  
Patient’S Outcome ◽  
Sampling Times

Cerebral vasospasm is a characteristic complication after subarachnoid hemorrhage (SAH), and the onset of vasospasm is a very important factor to decide the patient's outcome. Though various causal factors have been proposed for cerebral vasospasm after SAH, none of them explain the whole pathomechanism of vasospasm. To evaluate the role of trace elements in vasospasm, we have examined the sequential change in element concentration in the cerebrospinal fluid (CSF) after SAH by PIXE, and have investigated the relation between trace elements and vasospasm. We obtained the CSF samples from cisternal drainage of 17 patients with SAH who underwent radical surgery within 48 hours from the onset. The drainage was placed into basal cisterns at the end of the operation. Three sampling times (3-5, 7-9 and 12-14 days from the onset) were scheduled, because vasospasm is likely to occur from day 4 through day 14 after the onset. Cerebral angiograms were performed to classify vasospasm on day 1 and 7 after the onset. We measured 29 elements in the CSF and focused on Ca and Mg levels in this study, since Ca -influx into the smooth muscle cells is a principal mechanism of muscle contraction, and the competition between Ca and Mg is closely related to the muscle contraction. We found a significantly lower levels of Mg in the CSF of patients with vasospasm on days 7-9 after the onset. These results suggest that Mg in the CSF possibly ameliorate vasoconstriction due to Ca in the pathomechanism of vasospasm.

Phosphoramidon prevents cerebral vasospasm following subarachnoid hemorrhage in dogs: The relationship to endothelin-1 levels in the cerebrospinal fluid

Life Sciences ◽  
1991 ◽  
Vol 49 (11) ◽  
pp. 841-848 ◽  
Author(s):  
Yasuo Matsumura ◽  
Ruriko Ikegawa ◽  
Yasunori Suzuki ◽  
Masanori Takaoka ◽  
Takeshi Uchida ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Endothelin 1 ◽  
The Relationship

Cerebrospinal Fluid Tenascin-C in Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

2011 ◽  
Vol 23 (4) ◽  
pp. 310-317 ◽  
Author(s):  
Hidenori Suzuki ◽  
Kenji Kanamaru ◽  
Masato Shiba ◽  
Masashi Fujimoto ◽  
Kyoko Imanaka-Yoshida ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Tenascin C

Source and cause of endothelin-1 release into cerebrospinal fluid after subarachnoid hemorrhage

1997 ◽  
Vol 87 (2) ◽  
pp. 287-293 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Robert J. Boock ◽  
John K. Afshar ◽  
Kathleen Clouse ◽  
Mima Bacic ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Plasma Levels ◽  
Transient Cerebral Ischemia ◽  
Content Type ◽  
Endothelin 1 ◽  
Fine Print

✓ Despite years of research, delayed cerebral vasospasm remains a serious complication of subarachnoid hemorrhage (SAH). Recently, it has been proposed that endothelin-1 (ET-1) mediates vasospasm. The authors examined this hypothesis in a series of experiments. In a primate model of SAH, serial ET-1 levels were measured in samples from the perivascular space by using a microdialysis technique and in cerebrospinal fluid (CSF) and plasma during the development and resolution of delayed vasospasm. To determine whether elevated ET-1 production was a direct cause of vasospasm or acted secondary to ischemia, the authors also measured ET-1 levels in plasma and CSF after transient cerebral ischemia. To elucidate the source of ET-1, they measured its production in cultures of endothelial cells and astrocytes exposed to oxyhemoglobin (10 µM), methemoglobin (10 µM), or hypoxia (11% oxygen). There was no correlation between the perivascular levels of ET-1 and the development of vasospasm or its resolution. Cerebrospinal fluid and plasma levels of ET-1 were not affected by vasospasm (CSF ET-1 levels were 9.3 ± 2.2 pg/ml and ET-1 plasma levels were 1.2 ± 0.6 pg/ml) before SAH and remained unchanged when vasospasm developed (7.1 ± 1.7 pg/ml in CSF and 2.7 ± 1.5 pg/ml in plasma). Transient cerebral ischemia evoked an increase of ET-1 levels in CSF (1 ± 0.4 pg/ml at the occlusion vs. 3.1 ± 0.6 pg/ml 4 hours after reperfusion; p < 0.05), which returned to normal (0.7 ± 0.3 pg/ml) after 24 hours. Endothelial cells and astrocytes in culture showed inhibition of ET-1 production 6 hours after exposure to hemoglobins. Hypoxia inhibited ET-1 release by endothelial cells at 24 hours (6.4 ± 0.8 pg/ml vs. 0.1 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05) and at 48 hours (6.4 ± 0.6 pg/ml vs. 0 ± 0.1 pg/ml, control vs. hypoxic endothelial cells; p < 0.05), but in astrocytes hypoxia induced an increase of ET-1 at 6 hours (1.5 ± 0.6 vs. 6.4 ± 1.1 pg/ml, control vs. hypoxic astrocytes; p < 0.05). Endothelin-1 is released from astrocytes, but not endothelial cells, during hypoxia and is released from the brain after transient ischemia. There is no relationship between ET-1 and vasospasm in vivo or between ET-1 and oxyhemoglobin, a putative agent of vasospasm, in vitro. The increase in ET-1 levels in CSF after SAH from a ruptured intracranial aneurysm appears to be the result of cerebral ischemia rather than reflecting the cause of cerebral vasospasm.

scholarly journals Concentrations of estradiol, progesterone and testosterone in sefrum and cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage correlate weakly with transcranial Doppler flow velocities

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jan Martin ◽  
Eva Plank ◽  
Bernhard Ulm ◽  
Jens Gempt ◽  
Maria Wostrack ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebrospinal Fluid ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Transcranial Doppler ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Blood Flow Velocities ◽  
Flow Velocities

Abstract Background The implication of the steroids estradiol, progesterone and testosterone in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH) has not been comprehensively assessed. In rodents, studies suggested beneficial effects of steroids on cerebral vasospasm after experimental SAH. Studies in humans are warranted, however, a general dilemma of human studies on neuroactive substances is that the brain is not directly accessible and that concentrations in the periphery may not adequately parallel concentrations in the central compartments. In the present study, concentrations of estradiol, progesterone and testosterone in serum and cerebrospinal fluid (CSF) of patients with aSAH were determined. Blood flow velocities in cerebral arteries were measured by transcranial Doppler sonography (TCD). The aim of this study was to evaluate the correlations between the cerebral blood flow velocities and levels of estradiol, progesterone and testosterone in CSF and serum. Results Samples of serum and CSF of 42 patients with aSAH were collected concomitantly daily or every other day via the arterial line and the external ventricular drainage for two weeks after the hemorrhage. Blood flow velocities in the cerebral arteries were determined by TCD. Total estradiol, progesterone and testosterone concentrations were measured by electro-chemiluminescence immunoassay. The strength of correlation was assessed by Spearman’s rank correlation coefficient. The correlation analysis revealed very weak correlations between cerebral blood flow velocities and concentrations of estradiol, progesterone and testosterone levels in both compartments with correlation coefficients below 0.2. Conclusions In humans with aSAH, merely very weak correlations between flow velocities in cerebral arteries and concentrations of estradiol, progesterone and testosterone in serum and CSF were demonstrated. These results suggest a limited influence of the respective steroids on cerebral vascular tone although vasodilatory effects were described in rodent studies. Thus, the implication of steroids in processes of neurological deterioration warrants further clarification.

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