Expression of intercellular adhesion molecule 1 (ICAM-1) on the cerebral artery following subarachnoid haemorrhage in rats

Handa, Yuji; Kaneko, Masanori; Tsuchida, Akira; Kobayashi, Hidenori; Kawano, Hirokazu; Kubota, T.

doi:10.1007/bf01404854

Cited by 93 publications

(48 citation statements)

References 29 publications

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“…IL-8 is an important immunological inflammatory regulatory factor. Many experiments and clinical studies suggested that the immunological inflammatory responses induced by SAH took part in the development of cerebral vasospasm [1,2] . The responses were also intimately associated with cerebral ischemia [6] .…”

Section: Discussionmentioning

confidence: 99%

“…Its pathogenesis, however, is still ambiguous, and no completely effective clinical therapy is available currently. The important effect of immunological inflammatory on vessel walls in the pathogenesis of vasospasm has been noticed in recent years [1,2] , but the researches about the mRNA expression change of the inflammatory factors in the cerebral vascular were scarcely reported.…”

Section: Introductionmentioning

confidence: 99%

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Expression change of interleukin-8 gene in rabbit basilar artery after subarachnoid hemorrhage

et al. 2007

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Objective To study the expression change of interleukin-8 (IL-8) gene in the basilar artery of rabbit and the effect of IL-8 on the development of cerebral vasospasm induced by experimental subarachnoid hemorrhage (SAH). Methods Thirty five healthy Japanese White Rabbits were randomly divided into saline-control group and experimental group. The experimental group was subdivided into four groups, representing day 1, 4, 7 and 14 after the first blood injection of SAH. The delayed cerebral vasospasm (DCVS) model was established by double injection of autologous blood into the cisterna magna. The expression change of cytokine IL-8 mRNA in the basilar artery was analyzed by RT-PCR. Results The expression of IL-8 gene increased on day 4-7 after the first blood injection of SAH compared with control (P < 0.001), and decreased to normal on day 14. The expression of IL-8 gene in the SAH groups were positively correlated with the degree of basilar artery stenosis (r = 0.642, P < 0.01). Conclusion The expression level of IL-8 gene in basilar arteries was intimately associated with the degree of cerebral vasospasm, suggesting that IL-8 may play an important role in the DCVS after SAH as an immunological inflammatory factor.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression change of interleukin-8 gene in rabbit basilar artery after subarachnoid hemorrhage

et al. 2007

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“…Three adhesion molecules (E-selectin, ICAM-1, VCAM-1) were found to be elevated in CSF in patients having recently suffered an aneurismal SAH, with severely increased levels of E-selectin in those who later developed clinical VS (218). Expression of ICAM-1 was found to be increased in rat basilar artery not only in the endothelial layer but also in the media at 2 -5 days after SAH (219). However, Osuka et al (220) did not find increased levels of soluble ICAM-1 or VCAM-1 after SAH.…”

Section: Adhesion Molecule Expressionmentioning

confidence: 90%

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

181

137

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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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“…Studies in rats have yielded conflicting results about the timing of endothelial ICAM-I expression following haemorrhage 9,10. In a rat femoral artery model of post-haemorrhagic vasospasm, Sills et al reported that endothelial expression of ICA M-I was present between three and 24 hours post-haemorrhage, but ab-sent at 48 hours post-haemorrhage 9. In a rat SAH model, Handa et Al reported that endothelial expression of ICAM-I coincides with the peak of angiographic vasospasm in the basilar artery two to five days post-haemorrhage 10 . Differences in the timing of ICAM-I expression reported by these two studies may be related to regional differences in arterial physiology.…”

Section: Discussionmentioning

confidence: 99%

Timing of ICAM-I Expression in a Canine Model of Post-Haemorrhagic Cerebral Vasospasm

Abruzzo

Shengelaia²,

Cloft³

et al. 2000

Interv Neuroradiol

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Temporal alterations in endothelial intercellular adhesion molecule I (ICAM-I) expression during the course of post-haemorrhagic cerebral vasospasm (PHCV) are correlated with angiographic and histologic changes in the canine basilar artery. Angiography was performed in six dogs to obtain baseline measurements of basilar artery diameter. In three dogs subarachnoid haemorrhage (SAH) was created by performing percutaneous puncture of the cisterna magna, and replacing 7 ml of cerebrospinal fluid with 7 ml of arterial blood. The remaining three dogs were used as controls. Daily angiography was performed on all dogs to determine the percent reduction in basilar artery diameter (%RBAD). One dog from each group was sacrificed after 24 hours. The remaining two dogs in each group were sacrificed after 48 hours. Each basilar artery was perfusion fixed and subjected to histologic, and immunohistochemical analysis. In the SAH group, the average %RBAD was 4 (+/- 3) at 24 hours, and 36 (+/- 1) at 48 hours. In the control group, the average %RBAD was — 1 (+/- 1) at 24 hours, and 0 (+/- 2) at 48 hours. Endothelial edema and endothelial expression of ICAM-I were found at 24 hours. At 48 hours post-SAH there was widespread endothelial desquamation, but no evidence of ICAM-I expression. In the control group, histology was normal and no ICAM-I expression was found at 24 or 48 hours. The results suggest that a brief window of therapeutic efficacy exists during the first postictal 24 hours where ICAM-I antagonists may be useful in suppressing the pathogenesis of PHCV.

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Expression of intercellular adhesion molecule 1 (ICAM-1) on the cerebral artery following subarachnoid haemorrhage in rats

Cited by 93 publications

References 29 publications

Expression change of interleukin-8 gene in rabbit basilar artery after subarachnoid hemorrhage

Expression change of interleukin-8 gene in rabbit basilar artery after subarachnoid hemorrhage

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Timing of ICAM-I Expression in a Canine Model of Post-Haemorrhagic Cerebral Vasospasm

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