Structural changes and recovery of function after arterial injury.

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.

Effect of Saireitoh on Rabbit Smooth Muscle Cell Proliferation and Experimental Atherosclerosis

“…The accumulation of cholesterol in the arterial vessel wall is a prominent feature of atherosclerosis. Arterial intimal thickening induced after endothelial denudation by means of a balloon catheter is one of the most commonly used experimental models for a developing atheromatous plaque (4)(5)(6)(7)(8). Intimal thickening is mainly due to the migration of SMC into the intima and the proliferation of these cells mediated by various inflammatory cytokines and growth factors that have been released by inflammatory cells or synthesized within the arterial wall (9,10).…”

A new method to denude the endothelium without damage to media: structural, functional, and biomechanical validation

“…The endothelium is the largest autocrine, paracrine, and endocrine organ that regulates vessel tone, monocyte adhesion, platelet activation, thrombogenesis, inflammation, lipid metabolism, vessel growth, and remodeling (21, 23). Because endothelial injury is an important risk factor for atherosclerosis, numerous models of endothelial injury have appeared in the literature (10,12,13). Previous investigations have induced endothelial injury mechanically (via balloon distension, microsurgical instrument, or air desiccation) or chemically (via hydrochloric acid or Triton X-100) (2, 12).…”

“…The most widely used model, however, is injury induced by a balloon overinflated into the lumen of the vessel and dragged along the lumen to scrape off the endothelium. Unfortunately, this technique not only damages the endothelium but also the media including the smooth muscle cells and elastin fibers (9,12,13). Many of the previous studies using balloon injury purposely intended to model angioplasty.…”

“…Because endothelial injury is an important risk factor for atherosclerosis, numerous models of endothelial injury have appeared in the literature (10,12,13). Previous investigations have induced endothelial injury mechanically (via balloon distension, microsurgical instrument, or air desiccation) or chemically (via hydrochloric acid or Triton X-100) (2,12). The most widely used model, however, is injury induced by a balloon overinflated into the lumen of the vessel and dragged along the lumen to scrape off the endothelium.…”

Abundance of Plaque Microvessels is Associated With Constrictive Remodeling in Angioplastied Human Coronary Arteries.

“…18,19 For example, Langille and O'Donnell demonstrated in rabbit carotid arteries that decreased blood flow results in narrowing of the vessel diameter that is unchanged with papaverine and likely caused by structural changes in the artery wall. 18 However, when the endothelium is removed from these vessels the response to reduced blood flow is abolished.…”