A Nonhuman Primate Model of Delayed Cerebral Vasospasm After Aneurismal Subarachnoid Hemorrhage

2016 ◽  
pp. 227-250
Author(s):  
Ryszard M. Pluta ◽  
John Bacher ◽  
Boris Skopets ◽  
Victoria Hoffmann
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Nonhuman Primate ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
Delayed Cerebral Vasospasm

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.

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.

Maternal High-Fat Diet Persistently Alters Bone Marrow Immune Cell Proportions and Function in a Nonhuman Primate Model

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 222-OR
Author(s):  
MICHAEL J. NASH ◽  
TAYLOR K. SODERBORG ◽  
RACHEL C. JANSSEN ◽  
ERIC M. PIETRAS ◽  
JACOB E. FRIEDMAN
Keyword(s):  
Bone Marrow ◽  
Nonhuman Primate ◽  
High Fat Diet ◽  
Immune Cell ◽  
High Fat ◽  
Nonhuman Primate Model ◽  
Primate Model ◽  
And Function

scholarly journals Reperfusion plus Selective Intra-arterial Cooling (SI-AC) Improve Recovery in a Nonhuman Primate Model of Stroke

2020 ◽  
Author(s):  
Di Wu ◽  
Yongjuan Fu ◽  
Longfei Wu ◽  
Mitchell Huber ◽  
Jian Chen ◽  
...  
Keyword(s):  
Nonhuman Primate ◽  
Nonhuman Primate Model ◽  
Primate Model

Robotic Assessment of Upper Limb Function in a Nonhuman Primate Model of Chronic Stroke

2021 ◽  
Author(s):  
Yining Chen ◽  
Meredith C. Poole ◽  
Shelby V. Olesovsky ◽  
Allen A. Champagne ◽  
Kathleen A. Harrison ◽  
...  
Keyword(s):  
Upper Limb ◽  
Nonhuman Primate ◽  
Chronic Stroke ◽  
Nonhuman Primate Model ◽  
Limb Function ◽  
Primate Model ◽  
Upper Limb Function

scholarly journals Transcriptomic phases of periodontitis lesions using the nonhuman primate model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jeffrey L. Ebersole ◽  
Radhakrishnan Nagarajan ◽  
Sreenatha Kirakodu ◽  
Octavio A. Gonzalez
Keyword(s):  
Gene Expression ◽  
Nonhuman Primate ◽  
Gingival Crevicular Fluid ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Lesion Detection ◽  
Gingival Tissue ◽  
Specific Gene ◽  
Nonhuman Primate Model ◽  
Primate Model

AbstractWe used a nonhuman primate model of ligature-induced periodontitis to identify patterns of gingival transcriptomic after changes demarcating phases of periodontitis lesions (initiation, progression, resolution). A total of 18 adult Macaca mulatta (12–22 years) had ligatures placed (premolar, 1st molar teeth) in all 4 quadrants. Gingival tissue samples were obtained (baseline, 2 weeks, 1 and 3 months during periodontitis and at 5 months resolution). Gene expression was analyzed by microarray [Rhesus Gene 1.0 ST Array (Affymetrix)]. Compared to baseline, a large array of genes were significantly altered at initiation (n = 6049), early progression (n = 4893), and late progression (n = 5078) of disease, with the preponderance being up-regulated. Additionally, 1918 genes were altered in expression with disease resolution, skewed towards down-regulation. Assessment of the genes demonstrated specific profiles of epithelial, bone/connective tissue, apoptosis/autophagy, metabolism, regulatory, immune, and inflammatory responses that were related to health, stages of disease, and tissues with resolved lesions. Unique transcriptomic profiles occured during the kinetics of the periodontitis lesion exacerbation and remission. We delineated phase specific gene expression profiles of the disease lesion. Detection of these gene products in gingival crevicular fluid samples from human disease may contribute to a better understanding of the biological dynamics of the disease to improve patient management.

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