Electronegative LDL From Normolipemic Subjects Induces IL-8 and Monocyte Chemotactic Protein Secretion by Human Endothelial Cells

Abstract

Repair and remodeling processes initiated by arterial injury are thought to be critical in the pathogenesis of important vascular disorders. However, how these processes are related to specific types of injury is not well defined. Consequently, we compared arterial responses to several types of injury. Segments of rabbit carotid arteries were injured by intraluminal passage of an inflated embolectomy catheter, by hyperdistending the arteries with sterile saline, or by flushing them briefly with Triton X-100. Ballooning and Triton treatment removed the endothelium while imposing hyperdistending or nonhyperdistending injury on the vessel media. Hyperdistension with sterile saline caused medial injury but only transient and focal endothelial denudation. All modes of injury caused medial damage that was repaired within 2-7 days as assessed by vessel wall DNA content and synthesis and by capacity to contract. In addition, ballooned arteries recovered their capacity to exhibit diameter reductions induced by decreased blood flow once the endothelium had regenerated. The two injuries that caused endothelial denudation, ballooning and Triton treatment, resulted in equal intimal thickening after 6 weeks despite lower short- and long-term rates of cell replication after Triton-induced injury. Only ballooning resulted in chronic turnover of intimal smooth muscle cells after injury. No neointimal proliferation followed hyperdistension with saline despite significant medial injury. These latter findings suggest that even severe medial injury does not lead to intimal proliferation in the absence of endothelial denudation.