Serum monocyte chemoattractant protein-1 levels in rat models of intimal hyperplasia

Postoperative intimal hyperplasia is still the major cause of vein graft occlusion. No medicine, however, can suppress the development of postoperative intimal hyperplasia. Since June 2001, edaravone has been commercially available as the free radical scavenger for acute cerebral infarction. In addition, it is well known that edaravone in lower dosage also suppresses injury to endothelial cells of vessels in vitro. In this study we evaluated the effect of edaravone on the development of postoperative intimal hyperplasia in a rat model. In ten male rats (498 ± 53 g) we interposed the right epigastric vein graft into the common femoral artery. The ten rats were divided into two groups: edaravone group (n = 5) in which there was the preoperaiive administration of edaravone (3.0 mg/kg) into peritoneal cavity, and the control (n = 5) in which the same dose of saline was used. After 4 weeks three sections were taken from the vein grafts and stained with VerhoeffÕs and van GiesonÕs stains. The intimal areas of the vein graft were measured using computerized planimetry. The averages of the intimal area and serum monocyte chemoattractant protein 1 (MCP-1) level were compared between the two groups.The mean ischemic time was 68 ± 6 min. The average of the intimal area in the edaravone group was significantly lower than the control group (0.05 ± 0.02 mm 2 vs. 0.43 ± 0.05 mm 2 , p < 0.001). The average of serum MCP-1 in the edaravone group was also significantly lower than that of the control group (116 ± 11 pg/mL. vs. 169 ± 10 pg/mL, p < 0.01). Our results suggested that edaravone could suppress postoperative intimal hyperplasia of the vein graft in a rat model.

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Suppression of postoperative intimal hyperplasia of vein graft with edaravone in a rat model

Yamamura

Miyamoto

Mitsuno

et al. 2011

Int J Angiol

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Monocyte Chemoattractant Protein-1 Expression in Intimal Hyperplasia of Vein Grafts in a Rat Model

2002

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Realistic Temporal Variations of Shear Stress Modulate MMP-2 and MCP-1 Expression in Arteriovenous Vascular Access

et al. 2009

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Venous neointimal hyperplasia (VNH) lesions are prone to localized development within the vascular access junction (VAJ) and efferent vein of arteriovenous (AV) fistulae and grafts. The creation of VAJ dramatically alters the local venous hemodynamics with high pulsatile flow velocities enter the vein resulting in blood-flow separation, recirculation and flow reversal. This study conducted a computational hemodynamic investigation of an idealized AV graft and realistic AV fistula which demonstrated a complex hemodynamic environment within the VAJ, producing elevated wall shear stress (WSS) magnitudes and significant spatial and temporal WSS gradients in the VAJ. These hemodynamic patterns and non-physiological WSSs are postulated to initiate VNH development at the transcriptional level. Human umbilical vein endothelial cells (HU-VEC) were exposed to elevated temporal WSS waveforms obtained from the aforementioned computational analysis, using a cone-and-plate bioreactor. Using real-time RT-PCR, early induction of MMP-2 and delayed transcriptional upregulation of MCP-1 was observed following EC exposure to VAJ high wall shear forces. These results indicate that MMP-2 and MCP-1 may be induced by high WSS present in the VAJ, suggesting a link between elevated WSS magnitudes and temporal gradients, extracellular matrix decomposition, smooth muscle cell migration and proliferation, and the subsequent VNH development in AV VAJs.

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Serum monocyte chemoattractant protein-1 levels in rat models of intimal hyperplasia

Cited by 4 publications

References 6 publications

Suppression of postoperative intimal hyperplasia of vein graft with edaravone in a rat model

Suppression of postoperative intimal hyperplasia of vein graft with edaravone in a rat model

Monocyte Chemoattractant Protein-1 Expression in Intimal Hyperplasia of Vein Grafts in a Rat Model

Realistic Temporal Variations of Shear Stress Modulate MMP-2 and MCP-1 Expression in Arteriovenous Vascular Access

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