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Increasing levels of leukocyte-derived inflammatory mediators in plasma and cAMP in platelets during follow-up after acute cerebral ischemia

Anwaar, I. ; Gottsäter, A. LU ; Ohhson, K. ; Mattiasson, I LU and Lindgärde, Folke LU (1998) In Cerebrovascular Diseases 8(6). p.310-317
Abstract

Inflammatory mediators secreted by activated leukocytes play a role in the pathogenesis of atherosclerosis. They may also affect the production of vasodilatory and platelet antiaggregatory factors such as nitric oxide (NO) and prostacyclin (PGI2) from the vascular endothelium. Production of NO and PGI2, the effecs of which are mediated by cyclic 3',5'-guanosine monophosphate (cGMP) and cyclic 3',5'-adenosine monophosphate (cAMP), respectively, is disturbed in atherosclerosis, whereas increased NO levels have been found in acute cerebral ischemia. To investigate leukocyte activation and its possible influence upon endothelial function in cerebral ischemia we measured plasma neutrophil gelatinase-associated lipocalin... (More)

Inflammatory mediators secreted by activated leukocytes play a role in the pathogenesis of atherosclerosis. They may also affect the production of vasodilatory and platelet antiaggregatory factors such as nitric oxide (NO) and prostacyclin (PGI2) from the vascular endothelium. Production of NO and PGI2, the effecs of which are mediated by cyclic 3',5'-guanosine monophosphate (cGMP) and cyclic 3',5'-adenosine monophosphate (cAMP), respectively, is disturbed in atherosclerosis, whereas increased NO levels have been found in acute cerebral ischemia. To investigate leukocyte activation and its possible influence upon endothelial function in cerebral ischemia we measured plasma neutrophil gelatinase-associated lipocalin (NGAL) and soluble tumor necrosis factor receptor protein-1 (sTNFR-1) by ELISA, and intraplatelet cAMP and cGMP by radioimmunoassay in 59 patients with acute ischemic stroke or transient ischemic attack (mean age 71 years, 27 males) and after a 1-year follow-up in 57/59 (97%) patients. NGAL (152 ± 58 vs. 126 ± 48 μg/l), sTNFR-1 (3.50 ± 2.2 vs. 2.59 ± 1.31 μg/l), and cAMP(5.12 ± 1.71 vs. 4.06 ± 0.92 pmol/109 platelets) were higher (p < 0.001) after follow-up than in acute cerebral ischemia. At follow-up sTNFR-1 and cGMP partially correlated (r = 0.31; p < 0.05), controlling for age and platelet count. In conclusion, plasma NGAL and sTNFR-1 and intraplatelet AMP increase after acute cerebral ischemia, indicating chronic inflammatory activity and endothelial activation. Plasma sTNFR-1 levels are related to intraplatelet cGMP levels.

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author
; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
cAMP, Cerebral ischemia, Cytokines, Stroke
in
Cerebrovascular Diseases
volume
8
issue
6
pages
8 pages
publisher
Karger
external identifiers
  • pmid:9774747
  • scopus:0031754132
ISSN
1015-9770
DOI
10.1159/000015873
language
English
LU publication?
yes
id
037e17d6-8166-4fcf-ac03-c5709fc46e94
date added to LUP
2020-12-11 14:24:17
date last changed
2024-01-03 00:46:37
@article{037e17d6-8166-4fcf-ac03-c5709fc46e94,
  abstract     = {{<p>Inflammatory mediators secreted by activated leukocytes play a role in the pathogenesis of atherosclerosis. They may also affect the production of vasodilatory and platelet antiaggregatory factors such as nitric oxide (NO) and prostacyclin (PGI<sub>2</sub>) from the vascular endothelium. Production of NO and PGI<sub>2</sub>, the effecs of which are mediated by cyclic 3',5'-guanosine monophosphate (cGMP) and cyclic 3',5'-adenosine monophosphate (cAMP), respectively, is disturbed in atherosclerosis, whereas increased NO levels have been found in acute cerebral ischemia. To investigate leukocyte activation and its possible influence upon endothelial function in cerebral ischemia we measured plasma neutrophil gelatinase-associated lipocalin (NGAL) and soluble tumor necrosis factor receptor protein-1 (sTNFR-1) by ELISA, and intraplatelet cAMP and cGMP by radioimmunoassay in 59 patients with acute ischemic stroke or transient ischemic attack (mean age 71 years, 27 males) and after a 1-year follow-up in 57/59 (97%) patients. NGAL (152 ± 58 vs. 126 ± 48 μg/l), sTNFR-1 (3.50 ± 2.2 vs. 2.59 ± 1.31 μg/l), and cAMP(5.12 ± 1.71 vs. 4.06 ± 0.92 pmol/10<sup>9</sup> platelets) were higher (p &lt; 0.001) after follow-up than in acute cerebral ischemia. At follow-up sTNFR-1 and cGMP partially correlated (r = 0.31; p &lt; 0.05), controlling for age and platelet count. In conclusion, plasma NGAL and sTNFR-1 and intraplatelet AMP increase after acute cerebral ischemia, indicating chronic inflammatory activity and endothelial activation. Plasma sTNFR-1 levels are related to intraplatelet cGMP levels.</p>}},
  author       = {{Anwaar, I. and Gottsäter, A. and Ohhson, K. and Mattiasson, I and Lindgärde, Folke}},
  issn         = {{1015-9770}},
  keywords     = {{cAMP; Cerebral ischemia; Cytokines; Stroke}},
  language     = {{eng}},
  number       = {{6}},
  pages        = {{310--317}},
  publisher    = {{Karger}},
  series       = {{Cerebrovascular Diseases}},
  title        = {{Increasing levels of leukocyte-derived inflammatory mediators in plasma and cAMP in platelets during follow-up after acute cerebral ischemia}},
  url          = {{http://dx.doi.org/10.1159/000015873}},
  doi          = {{10.1159/000015873}},
  volume       = {{8}},
  year         = {{1998}},
}