Inducible Cyclooxygenase Expression in Canine Basilar Artery After Experimental Subarachnoid Hemorrhage

Osuka, Koji; Suzuki, Yoshio; Watanabe, Yasuo; Takayasu, Misako; Yoshida, Jun

doi:10.1161/01.str.29.6.1219

Cited by 39 publications

(21 citation statements)

References 44 publications

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“…In the cerebral arteries COX-2 is expressed constitutionally (113), but its overexpression after SAH has been little studied. In an immunohistochemical study, it was found only in the endothelial layer 3 days after SAH (91), although a previous immunoblot study showed its overexpression in the arteries after 2 days (114). In our study (91), the expression of COX-2 was preceded during day 1 by a rise in the CSF concentration of TNF-a .…”

Section: The 5-lipoxygenase Pathway and Ltscontrasting

confidence: 52%

“…These findings suggest that IL-1b is a powerful molecule acting at very low concentrations. Intracisternal injection of cytokines (0.03 mg IL-1b, 3 mg IL-6 or 10 mg IL-8) induce COX-2-immunoreactive protein in the basilar artery (114).…”

Section: Il-1mentioning

confidence: 99%

“…IL-8 could play a role in the pathophysiology of VS by stimulating the COX cascade. IL-8 has been shown to induce a COX-2-like protein in canine basilar artery within 12 h after intracisternal injection (114) and to stimulate human aortic SMCs to produce PGE 2 . Moreover, canine spastic basilar arteries showed an increased mRNA expression for IL-8 (222), but IL-8 alone seems unable to generate vasoconstriction (220).…”

Section: Il-8 and Mcp-1mentioning

confidence: 99%

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Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

182

140

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ABSTRACT-Aneurysmal subarachnoid hemorrhage frequently results in complications including intracranial hypertension, rebleeding and vasospasm. The extravasated blood is responsible for a cascade of reactions involving release of various vasoactive and pro-inflammatory factors (several of which are purported to induce vasospasm) from blood and vascular components in the subarachnoid space. The authors review the available evidence linking these factors to the development of inflammatory lesions of the cerebral vasculature, emphasizing: 1) neurogenic inflammation due to massive release of sensory nerve neuropeptides; 2) hemoglobin from lysed erythrocytes, which creates functional lesions of endothelial and smooth muscle cells; 3) activity, expression and metabolites of lipoxygenases cyclooxygenases and nitric oxide synthases; 4) the possible role of endothelin-1 as a pro-inflammatory agent; 5) serotonin, histamine and bradykinin which are especially involved in blood-brain barrier disruption; 6) the prothrombotic and pro-inflammatory action of complement and thrombin towards endothelium; 7) the multiple actions of activated platelets, including platelet-derived growth factor production; 8) the presence of perivascular and intramural macrophages and granulocytes and their interaction with adhesion molecules; 9) the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-a and IL-6. Human and animal studies on the use of anti-inflammatory agents in subarachnoid hemorrhage include superoxide and other radical scavengers, lipid peroxidation inhibitors, iron chelators, NSAIDs, glucocorticoids, and serine protease inhibitors. Many animal studies claim reduced vasospasm, but these effects are not always confirmed in human trials, where symptomatic vasospasm and outcome are the major endpoints. Despite recent work on penetrating vessel constriction, there is a paucity of studies on inflammatory markers in the microcirculation.

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Section: The 5-lipoxygenase Pathway and Ltscontrasting

confidence: 52%

Section: Il-1mentioning

confidence: 99%

Section: Il-8 and Mcp-1mentioning

confidence: 99%

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Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

182

140

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“…The elevation of COX-2 in the cerebral arteries after SAH has been previously described (42,43,53). COX-2 produces a variety of vasoactive prostanoids as well as superoxide anion that may have affected the baseline diameter as well as the responsiveness of the basilar artery to both acetylcholine and cromakalim.…”

Section: Discussionmentioning

confidence: 72%

Impaired vascular responses of insulin-resistant rats after mild subarachnoid hemorrhage

Institóris

Snipes

Katakam

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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DW. Impaired vascular responses of insulinresistant rats after mild subarachnoid hemorrhage. Am J Physiol Heart Circ Physiol 300: H2080 -H2087, 2011. First published March 18, 2011 doi:10.1152/ajpheart.01169.2010.-Insulin resistance (IR) impairs cerebrovascular responses to several stimuli in Zucker obese (ZO) rats. However, cerebral artery responses after subarachnoid hemorrhage (SAH) have not been described in IR. We hypothesized that IR worsens vascular reactions after a mild SAH. Hemolyzed blood (300 l) or saline was infused (10 l/min) into the cisterna magna of 11-13-wk-old ZO (n ϭ 25) and Zucker lean (ZL) rats (n ϭ 25). One day later, dilator responses of the basilar artery (BA) and its side branch (BA-Br) to acetylcholine (ACh, 10 Ϫ6 M), cromakalim (10 Ϫ7 M, 10 Ϫ6 M), and sodium nitroprusside (10 Ϫ7 M) were recorded with intravital videomicroscopy. The baseline diameter of the BA was increased both in the ZO and ZL rats 24 h after the hemolysate injection. Saline-injected ZO animals showed reduced dilation to ACh (BA ϭ 9 Ϯ 3 vs. 22 Ϯ 4%; and BA-Br ϭ 23 Ϯ 5 vs. 37 Ϯ 7%) compared with ZL rats. Hemolysate injection blunted the response to ACh in both the ZO (BA ϭ 4 Ϯ 2%; and BA-Br ϭ 12 Ϯ 3%) and ZL (BA ϭ 7 Ϯ 2%; and BA-Br ϭ 11 Ϯ 3%) rats. Cromakalim (10 Ϫ6 M)-induced dilation was significantly reduced in the hemolysate-injected ZO animals compared with the saline control (BA ϭ 13 Ϯ 3 vs. 26 Ϯ 5%; and BA-Br ϭ 28 Ϯ 8 vs. 44 Ϯ 9%) and in the hemolysate-injected ZL rats compared with their saline control (BA ϭ 24 Ϯ 4 vs. 32 Ϯ 4%; but not BA-Br ϭ 39 Ϯ 6 vs. 59 Ϯ 9%). No significant difference in sodium nitroprusside reactivity was observed. Western blot analysis of the BA showed a lower baseline level of neuronal nitric oxide synthase expression and an enhanced cyclooxygenase-2 level in the hemolysate-injected ZO animals. In summary, cerebrovascular reactivity to both endothelium-dependent and -independent stimuli is severely compromised by SAH in IR animals. cerebral circulation; endothelium; vascular smooth muscle; nitric oxide; Zucker obese rats; adenosine 5=-triphosphate-sensitive potassium channels; insulin resistance INSULIN RESISTANCE (IR), a normally "silent" and undetected predecessor of type II diabetes, is a major risk factor for the development of cerebral vascular disease and neurological pathologies such as strokes. There is an increased prevalence of both ischemic and hemorrhagic strokes in IR individuals (4,14,45,56), and stroke patients with type 2 diabetes experience a slower recovery of neurological function and a higher mortality (2, 3, 23, 55). The major underlying basis for augmented neurological damage could be the IR-related dysfunction of the cerebral vasculature. The leptin receptor-deficient Zucker obese (ZO) rat is a commonly used animal model to study IR. The 11-13-wk-old prediabetic ZO rat is characterized by obesity, normal blood pressure, and elevated plasma insulin and lipid levels, without an increase of glucose level. Our laboratory made the original observations that dilator r...

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“…The release of prostaglandins is part of the inflammatory response and may mediate tissue inflammation or anti-inflammatory effects (21). COX-2 expression was detected in basilar arterial tissue in both acute and chronic stages following SAH (22). Therefore, PGES may, in turn, produce sufficient quantities of eicosanoids to affect hemodynamics following SAH.…”

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confidence: 99%

Immune and inflammatory gene signature in rat cerebrum in subarachnoid hemorrhage with microarray analysis

et al. 2011

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Abstract. Cerebral vasospasm following subarachnoid hemorrhage (SAH) has been studied in terms of a contraction of the major cerebral arteries, but the effect of cerebrum tissue in SAH is not yet well understood. To gain insight into the biology of SAH-expressing cerebrum, we employed oligonucleotide microarrays to characterize the gene expression profiles of cerebrum tissue at the early stage of SAH. Functional gene expression in the cerebrum was analyzed 2 h following stage 1-hemorrhage in Sprague-Dawley rats. mRNA was investigated by performing microarray and quantitative real-time PCR analyses, and protein expression was determined by Western blot analysis. In this study, 18 upregulated and 18 downregulated genes displayed at least a 1.5-fold change. Five genes were verified by real-time PCR, including three upregulated genes [prostaglandin E synthase (PGES), CD14 antigen, and tissue inhibitor of metalloproteinase 1 (TIMP1)] as well as two downregulated genes [KRAB-zinc finger protein-2 (KZF-2) and γ-aminobutyric acid B receptor 1 (GABA B receptor)]. Notably, there were functional implications for the three upregulated genes involved in the inflammatory SAH process. However, the mechanisms leading to decreased KZF-2 and GABA B receptor expression in SAH have never been characterized. We conclude that oligonucleotide microarrays have the potential for use as a method to identify candidate genes associated with SAH and to provide novel investigational targets, including genes involved in the immune and inflammatory response. Furthermore, understanding the regulation of MMP9/TIMP1 during the early stages of SAH may elucidate the pathophysiological mechanisms in SAH rats.

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Inducible Cyclooxygenase Expression in Canine Basilar Artery After Experimental Subarachnoid Hemorrhage

Cited by 39 publications

References 44 publications

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Impaired vascular responses of insulin-resistant rats after mild subarachnoid hemorrhage

Immune and inflammatory gene signature in rat cerebrum in subarachnoid hemorrhage with microarray analysis

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