Natriuretic peptide system and endothelin in aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 87 (2) ◽  
pp. 275-280 ◽  
Author(s):  
Eelco F. M. Wijdicks ◽  
Wouter I. Schievink ◽  
John C. Burnett
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Natriuretic Peptide ◽  
Cerebral Vasospasm ◽  
Fluid Balance ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Peptide System ◽  
Natriuretic Peptide System ◽  
Fine Print

✓ The natriuretic peptide system consists of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The system is implicated in the control of body fluid homeostasis, causes natriuresis and diuresis (ANP and BNP), and regulates vascular tone (CNP). A reciprocal relationship between ANP and endothelin (ET) has been suggested, and earlier studies have documented a possible role of ET in cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The authors studied plasma ANP, BNP, CNP, and ET for 6 consecutive days in 13 patients with SAH by using radioimmunoassay. The median admission values for ANP were 31.5 pg/ml (range 16.8–323 pg/ml [normal 15 ± 7 pg/ml]); for BNP, 45.3 pg/ml (range 2.2–80.2 pg/ml [normal 12 ± 9 pg/ml]); for CNP, 7.7 pg/ml (range < 2–20 pg/ml [normal 5.2 ± 3 pg/ml]); and for ET, 11 pg/ml (range 6.5–25.1 pg/ml [normal 7.2 ± 4 pg/ml]). Additional increases (defined as > 100% increase on two consecutive measurements) were noted in ANP (11 patients), BNP (10 patients), and CNP (three patients), and resulted in a negative fluid balance in 10 of the 13 patients. The CNP increased in three of four patients with cerebral vasospasm and in one of nine patients without cerebral vasospasm (Fisher's exact test, p = 0.2). No major fluctuations in plasma ET were noted. In seven patients, the plasma ET level did not increase beyond 10 pg/ml during the days of measurement. In six patients, only an occasional sample showed an increase to a maximum of 25 pg/ml. Changes in BNP, ANP, and CNP were independent of each other. The authors conclude that both plasma ANP and BNP increase after SAH and often result in a negative fluid balance. Plasma ANP and BNP seem differentially regulated in the presence of SAH but not by the level of the plasma ET. The possible role of CNP as a regulatory response to cerebral vasospasm needs further exploration.

Increase and uncoupling of adrenomedullin from the natriuretic peptide system in aneurysmal subarachnoid hemorrhage

2001 ◽  
Vol 94 (2) ◽  
pp. 252-256 ◽  
Author(s):  
Eelco F. M. Wijdicks ◽  
Denise M. Heublein ◽  
John C. Burnett
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Natriuretic Peptide ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Doppler Studies ◽  
Content Type ◽  
Peptide System ◽  
The Mean ◽  
Cerebral Vasodilation ◽  
Natriuretic Peptide System ◽  
Fine Print

Object. Natriuresis is a common systemic manifestation of aneurysmal subarachnoid hemorrhage (SAH). Natriuresis and its accompanying hypovolemia may be a major contributing factor in the pathophysiology of symptomatic cerebral vasospasm. Methods. The authors studied 14 consecutive patients with aneurysmal SAH and compared levels of adrenomedullin (ADM), a novel endogenous natriuretic peptide that possesses additional profound vasodilatory properties, with the natriuretic peptide system by using radioimmunoassay. The mean ADM values on admission were 24.8 pg/ml, a twofold increase over control values, but no correlation was found with atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-natriuretic peptide (CNP) from the natriuretic peptide system. At Day 5 post-SAH, ADM levels were significantly elevated in patients with vasospasm documented angiographically or on transcranial Doppler studies as compared with those who suffered no vasospasm (mean 61.9 pg/ml compared with 15.3 pg/ml, p < 0.01). Conclusions. The authors conclude that an elevation of ADM in plasma may indicate a physiological regulatory attempt to induce cerebral vasodilation. The regulation of ADM is uncoupled from ANP, BNP, and CNP.

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.

Efficacy of transluminal angioplasty for the management of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2000 ◽  
Vol 92 (2) ◽  
pp. 284-290 ◽  
Author(s):  
Richard S. Polin ◽  
Volker A. Coenen ◽  
Carolyn Apperson Hansen ◽  
Peter Shin ◽  
Mustafa K. Baskaya ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Scale Score ◽  
Cerebral Vasospasm ◽  
Medical Management ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Conditional Logistic Regression ◽  
Study Drug ◽  
Transluminal Angioplasty ◽  
Content Type ◽  
Fine Print

Object. Transluminal angioplasty has become a widely used adjunct therapy to medical management of symptomatic cerebral vasospasm following subarachnoid hemorrhage (SAH). Despite anecdotal reports of universal, angiographically confirmed reversal of vasospasm and high rates of clinical improvement, no rigorous examination of the efficacy of this procedure has been conducted. In this study the authors assess the efficacy of the aforementioned procedure.Methods. Thirty-eight patients enrolled as part of the North American trial of tirilazad in aneurysmal SAH underwent transluminal angioplasty for symptomatic cerebral vasospasm. Fifty-three percent of these patients showed good recovery or moderate disability based on their 3-month Glasgow Outcome Scale score.Among the 38 patients who underwent angioplasty, the severity and type of vasospasm, use of papaverine in addition to balloon angioplasty, timing of treatment, and dose of study drug did not have an effect on the outcome. The results of their neurological examinations improved in only four of the 38 patients immediately after the procedure. A conditional logistic regression analysis was performed in which these patients were compared with individuals matched for age, sex, dose of study drug, admission neurological grade, and modified Glasgow Coma Scale score at the time of angioplasty. No effect on favorable outcomes was found for this procedure.Conclusions. Transluminal cerebral angioplasty is very effective in reversing angiographically confirmed vasospasm, and anecdotal reports of its clinical utility are numerous. However, in this report the authors conclude that its superiority to medical management for symptomatic cerebral vasospasm is questionable.

Neuropeptide Y in the primate model of subarachnoid hemorrhage

1992 ◽  
Vol 77 (3) ◽  
pp. 417-423 ◽  
Author(s):  
Ryszard M. Pluta ◽  
Anna Deka-Starosta ◽  
Alois Zauner ◽  
Jay K. Morgan ◽  
Karin M. Muraszko ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Neuropeptide Y ◽  
Cerebral Vasospasm ◽  
Primate Model ◽  
Content Type ◽  
Peripheral Plasma ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Plasma ◽  
Fine Print

✓ The cause of cerebral vasospasm after subarachnoid hemorrhage (SAH) remains unknown. Recently, an association between the potent vasoconstricting peptide, neuropeptide Y, and delayed cerebral vasospasm after SAH has been postulated. This was based on the findings of increased neuropeptide Y levels in the cerebrospinal fluid (CSF) and plasma after SAH in animals and humans. For this study, the primate model of SAH was used to assess the possible role of neuropeptide Y in delayed vasospasm after SAH. Fifteen cynomolgus monkeys underwent placement of a clot of either whole blood or red blood cells in the subarachnoid space around the middle cerebral artery (MCA). Sequential arteriography for assessment of MCA diameter and sampling of blood and CSF for neuropeptide Y were performed: before SAH (Day 0); 7 days after SAH, when signs of delayed cerebral vasospasm peak in this model and in humans; 12 days after SAH; and 28 days after SAH. Subarachnoid hemorrhage did not evoke changes in CSF or plasma levels of neuropeptide Y. Nine monkeys had arteriographic evidence of vasospasm on Day 7, but no change in neuropeptide Y levels occurred in plasma or CSF. In addition, neuropeptide Y levels did not change, even after resolution of vasospasm on Day 12 or Day 28. Neuropeptide Y levels were substantially higher in CSF than in arterial plasma (p < 0.003 at each interval). No correlation was found between neuropeptide Y levels in CSF and in plasma. These results do not confirm a relationship between neuropeptide Y levels in the CSF or peripheral plasma and delayed cerebral vasospasm in SAH.

A Pilot Study of Dendroaspis Natriuretic Peptide in Aneurysmal Subarachnoid Hemorrhage

Neurosurgery ◽  
2004 ◽  
Vol 55 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Vini G. Khurana ◽  
Eelco F.M. Wijdicks ◽  
Denise M. Heublein ◽  
Robyn L. McClelland ◽  
Fredric B. Meyer ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Natriuretic Peptide ◽  
Fluid Balance ◽  
Large Scale ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Venous Blood ◽  
Laboratory Data ◽  
Sodium Concentration ◽  
Peptide Family

Abstract OBJECTIVE: Hypovolemia after aneurysmal subarachnoid hemorrhage (SAH) may be mediated by natriuretic peptides and can further impair cerebral perfusion in dysau-toregulated and vasospastic arterial territories. Dendroaspis natriuretic peptide (DNP), derived from the venom of Dendroaspis augusticeps, the Green Mamba snake, has recently been discovered in human plasma and atrial myocardium. There is no information regarding the presence or putative role of this peptide in patients with aneurysmal SAH. METHODS: A sensitive and specific DNP radioimmunoassay was performed on venous blood samples obtained on post-SAH Days 1, 3, and 7 from 10 consecutive SAH patients (cases) and randomly from 9 healthy volunteers (controls). Clinical and laboratory data, including daily serum sodium concentration and fluid balance, were collected prospectively up to 7 days after the ictus. RESULTS: Increase in plasma DNP levels occurred in five (63%) of eight patients who had DNP levels measured on Days 1 and 3 (mean increase, 29%). An increase in DNP level was significantly associated with development of a negative fluid balance (P = 0.003) and hyponatremia (P = 0.008). Three (75%) of the four patients who developed cerebral vasospasm during this study experienced an increase in DNP levels from Days 1 to 3. CONCLUSION: The present study is the first to find a significant association between elevated levels of DNP, a new member of the natriuretic peptide family, and the development of diuresis and natriuresis in patients with aneurysmal SAH. Our findings warrant further investigation by means of a large-scale, prospective, case-control study.

Rise in serum soluble intercellular adhesion molecule—1 levels with vasospasm following aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (3) ◽  
pp. 537-541 ◽  
Author(s):  
J Mocco ◽  
William J. Mack ◽  
Grace H. Kim ◽  
Alan P. Lozier ◽  
Ilya Laufer ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Adhesion Molecule ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Intercellular Adhesion Molecule ◽  
Adhesion Molecule Expression ◽  
Intercellular Adhesion Molecule 1 ◽  
Content Type ◽  
Soluble Intercellular Adhesion Molecule ◽  
Fine Print

Object. Proinflammatory adhesion molecule expression has been demonstrated to be elevated in patients with aneurysmal subarachnoid hemorrhage (SAH). Recent studies have shown that elevations in soluble intercellular adhesion molecule—1 (ICAM-1) may be predictive of poor outcome in patients with good grade (Hunt and Hess Grades 1–2) aneurysmal SAH at delayed time points that correspond with the risk period for cerebral vasospasm. In addition, ICAM-1 is upregulated in experimental models of vasospasm. Unfortunately, the relationship of adhesion molecule expression to human vasospasm remains unclear. The authors hypothesized that the delayed elevation of soluble ICAM-1 in patients with aneurysmal SAH is associated with the development of cerebral vasospasm. Methods. Eighty-nine patients with aneurysmal SAH were prospectively enrolled in a study and stratified according to the presence or absence of vasospasm, as evidenced by daily monitoring of transcranial Doppler (TCD) velocities (presence, > 200 cm/second; absence, ≤ 120 cm/second). Levels of soluble ICAM-1 were determined using enzyme-linked immunosorbent assay every other day for 12 days post-SAH. An analysis of covariance model was used to evaluate trends in soluble ICAM-1 levels from 2 days prior to 6 days after the occurrence of documented vasospasm. Two groups of patients, matched for admission admission Hunt and Hess grade, were compared: nine patients with TCD velocities greater than 200 cm/second and nine patients with TCD velocities less than 120 cm/second. From among the patients with TCD velocities greater than 200 cm/second six patients with angiographically documented vasospasm were selected. Patients with TCD velocities less than 120 cm/second and matched admission Hunt and Hess grades but without angiographically documented vasospasm were selected. Patients with TCD-demonstrated vasospasm showed a significant mean rate of rise (p < 0.01) in soluble ICAM-1 levels during the perivasospasm period, but admission Hunt and Hess grade—matched control patients did not (p = not significant [NS]). There was a significant difference between these groups' rates of soluble ICAM increase (p < 0.01). Patients with both TCD- and angiographically demonstrated vasospasm likewise showed a highly significant mean rate of increase in soluble ICAM-1 levels during the perivasospasm period (p < 0.01), whereas admission Hunt and Hess grade—matched controls did not (p = NS). The difference beween these groups' rates of increase was highly significant (p < 0.001). Conclusions. These data suggest a role for ICAM-1 in the pathophysiology of cerebral vasospasm or its ischemic sequelae. As this relationship is further elucidated, adhesion molecules such as ICAM-1 may provide novel therapeutic targets in the prevention of vasospasm or its ischemic consequences.

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (6) ◽  
pp. 1222-1226 ◽  
Author(s):  
Matthew J. McGirt ◽  
John C. Mavropoulos ◽  
Laura Y. McGirt ◽  
Michael J. Alexander ◽  
Allan H. Friedman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Leukocyte Count ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Increased Risk ◽  
Grade 3 ◽  
Fine Print

Object. The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm. Methods. A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 ± 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5–15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02–1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01–0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04–0.45). A serum leukocyte count greater than 15 × 109/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74–6.38). Conclusions. During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 × 109/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

The role of hemoglobin in the etiology of cerebral vasospasm

1983 ◽  
Vol 59 (2) ◽  
pp. 231-236 ◽  
Author(s):  
David J. Boullin ◽  
Philip Tagari ◽  
George du Boulay ◽  
Victoria Aitken ◽  
J. Trevor Hughes
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Angiography ◽  
Aneurysm Rupture ◽  
Neurological Deficits ◽  
Arterial Spasm ◽  
Content Type ◽  
Experimental Animals ◽  
Fine Print

✓ Oxyhemoglobin was injected intracisternally into three baboons, and methemoglobin into one baboon, in an attempt to mimic the prolonged cerebral arterial spasm sometimes seen after subarachnoid hemorrhage due to aneurysm rupture. Cerebral angiography was performed for up to 7 days after injection of hemoglobin, and the degree of vasospasm was estimated from the angiograms. Oxyhemoglobin caused slight arterial narrowing, which lasted for 3 days. Methemoglobin had no significant effects. Motor neurological deficits and histopathological signs, characteristic of prolonged cerebral vasospasm, were not observed. It was concluded that hemoglobin alone is not capable of causing the cerebral vasospasm syndrome in these experimental animals.

Role of prostaglandin F2 in human cerebral vasospasm

1974 ◽  
Vol 41 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Emanuele La Torre ◽  
Carlo Patrono ◽  
Aldo Fortuna ◽  
Daniela Grossi-Belloni
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Experimental Work ◽  
Arterial Spasm ◽  
Control Series ◽  
Content Type ◽  
Serial Samples ◽  
Fine Print

✓Prostaglandin (PGF2α) concentrations were measured by radioimmunoassay in serial samples of CSF from patients with subarachnoid hemorrhage, in an attempt to correlate these values with the presence or degree of the arterial spasm. Although elevated concentrations of PGF2α were found in most of these patients, when compared with a control series, there was no correlation between these values and the appearance of cerebral vasospasm. The results are discussed with reference to previous experimental work suggesting a role of PGF2α in the pathogenesis of cerebral vasospasm.

The role of endothelin-1 in the origin of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage

1992 ◽  
Vol 77 (1) ◽  
pp. 96-100 ◽  
Author(s):  
Ryuta Suzuki ◽  
Hiroyuki Masaoka ◽  
Yukio Hirata ◽  
Fumiaki Marumo ◽  
Eiji Isotani ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Time Course ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Normal Range ◽  
Content Type ◽  
Patient Groups ◽  
Group 3 ◽  
Fine Print

✓ Plasma and cerebrospinal fluid (CSF) endothelin (ET)-1-like immunoactivity in 27 patients with aneurysmal subarachnoid hemorrhage (SAH) was measured serially by radioimmunoassay for 2 weeks after SAH onset. Mean ET-1-like immunoactivity levels in plasma of patients with SAH were highly elevated during the whole study period, while the levels in CSF of the same patients were not. Plasma ET-1-like immunoactivity levels in patients with SAH classified as Fisher computerized tomography (CT) Group 3 were higher than those in patients with SAH classified as Fisher CT Groups 1 and 2. There were no significant differences in plasma ET-1-like immunoactivity levels between the patient groups stratified by Hunt and Kosnik grade. In this series, plasma ET-1-like immunoactivity levels in the 12 patients with vasospasm were higher than those in the 15 patients without vasospasm during the 1st week; CSF ET-1-like immunoactivity levels in patients with vasospasm were in the normal range on Days 0 to 3 after SAH onset, then became elevated on Days 5 to 7 and remained high until the end of the 2nd week. In contrast, CSF ET-1-like immunoactivity levels in patients without vasospasm were within the normal range during the entire period of study. The time course of the occurrence of vasospasm and that of the increase in CSF ET-1-like immunoactivity coincided precisely. The possible role of endogenous ET-1 in the pathogenesis of vasospasm due to SAH is discussed.

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