HYALURONAN (HYAL-BV-5200) INHIBITS NEOINTIMAL MACROPHAGE INFLUX AFTER BALLOON-CATHETER INDUCED INJURY IN THE CHOLESTEROL-FED RABBIT

被引:24
作者
FERNS, GAA [1 ]
KONNEH, M [1 ]
RUTHERFORD, C [1 ]
WOOLAGHAN, E [1 ]
ANGGARD, EE [1 ]
机构
[1] UNIV LEICESTER, GLENFIELD GEN HOSP, DEPT CHEM PATHOL, LEICESTER LE3 9QP, LEICS, ENGLAND
关键词
RABBIT; CAROTID; HYALURONAN; ANGIOPLASTY; MACROPHAGE;
D O I
10.1016/0021-9150(94)05479-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Hyaluronan is a glycosaminoglycan, elaborated by several cell types, and is a major constituent of the extracellular matrix. Recent studies suggest that hyaluronan influences cell migration and proliferation. At high concentrations, it has been shown to inhibit macrophage migration in vitro. We have investigated the effects of hyaluronan administration on neo-intimal lesion development following balloon catheter injury of the common carotid artery in the cholesterol-fed New Zealand White rabbit. Hyaluronan, administered as sodium hyaluronate at the time of surgery and daily until sacrifice, 2 weeks later, reduced the absolute neo-intimal response to injury by 42% (117 +/- 16 mu m to 68 +/- 11 mu m; P < 0.05), and the intima-media ratio by 35% (0.91 +/- 0.10 to 0.59 +/- 0.11; P < 0.05). This was associated with a 62% reduction in intimal macrophage content (8.63 +/- 1.85% to 3.25 +/- 1.05%; P < 0.02). At the time of killing, serum cholesterol levels and weight gain were comparable between the groups of animals receiving a cholesterol diet (P > 0.05). In both groups mean serum cholesterol levels at the time of the balloon injury and killing were significantly greater than at entry (P < 0.001), and significantly higher than in a group receiving control chow (P < 0.001). These data suggest that the effect of hyaluronic acid on neo-intimal size may be mediated, in part, by an inhibition of monocyte/macrophage influx, and support the view that hyaluronan impairs monocyte migration.
引用
收藏
页码:157 / 164
页数:8
相关论文
共 30 条
[1]  
Leimgruber, Roubin, Hollman, Et al., Restenosis after successful coronary angioplasty in patients with single vessel disease, Circulation, 73, (1986)
[2]  
Glazier, Williams, Madden, Rickards, Clinical outcome following coronary balloon angioplasty in 100 consecutive patients with multivessel coronary artery disease, J R Coll Phys Lond, 24, (1990)
[3]  
Meier, Long term results of coronary balloon angioplasty, Annu Rev Med, 42, (1991)
[4]  
RITA trial. Coronary angioplasty versus coronary artery bypass surgery in the Randomized Intervention Treatment of Angina Trial, Lancet, (1993)
[5]  
Austin, Ratliff, Hollman, Tabei, Phillips, Intimal proliferation of smooth muscle cells as an explanation for recurrent coronary artery stenosis after percutaneous transluminal coronary angioplasty, J Am Coll Cardiol, 6, (1985)
[6]  
Waller, Pinkerton, Orr, Slack, Van Tassel, Peters, Morphological observations late (greater than 30 days) after clinically successful balloon coronary angioplasty, Circulation, 83, (1991)
[7]  
Clagett, Robinowitz, Youkey, Et al., Morphogenesis and clinicopathologic characteristics of recurrent carotid disease, J Vasc Surg, 3, (1986)
[8]  
Yla-Herttuala, Lipton, Rosenfeld, Et al., Expression of monocyte chemoattractant protein 1 in macrophage rich areas of human and rabbit atherosclerotic lesions, Proceedings of the National Academy of Sciences, 88, (1991)
[9]  
Raines, Ross, Macrophage-derived growth factors, Human Monocytes, pp. 247-259, (1989)
[10]  
Clowes, Reidy, Clowes, Kinetics of cellular proliferation after arterial injury. I. Smooth muscle cell growth in the absence of endothelium, Lab Invest, 49, (1983)