STRUCTURAL-CHANGES AND RECOVERY OF FUNCTION AFTER ARTERIAL INJURY

STRUCTURAL-CHANGES AND RECOVERY OF FUNCTION AFTER ARTERIAL INJURY
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DOI:
10.1161/01.atv.12.3.307
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发表时间:
1992-03-01
期刊:
ARTERIOSCLEROSIS AND THROMBOSIS
影响因子:
--
通讯作者:
LANGILLE, BL
LANGILLE, BL
中科院分区:
其他
文献类型:
--
作者:
JAMAL, A;BENDECK, M;LANGILLE, BL

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由动脉损伤引发的修复和重塑过程被认为在重要血管疾病的发病机制中至关重要。 然而,这些过程如何与特定类型的损伤有关还没有很好的定义。 因此,我们比较了动脉对几种类型损伤的反应。 兔颈动脉段损伤的管腔内通过膨胀的栓子切除导管,通过过度扩张的动脉与无菌生理盐水,或通过冲洗它们短暂的Triton X-100。 血管扩张和Triton处理去除内皮,同时对血管中膜施加过度扩张或非过度扩张损伤。 用无菌生理盐水过度扩张引起中膜损伤,但仅引起短暂的局灶性内皮剥脱。 所有损伤模式均引起中膜损伤,通过血管壁DNA含量和合成以及收缩能力评估,中膜损伤在2-7天内修复。 此外,一旦内皮再生,球囊扩张的动脉恢复了其表现出由血流减少引起的直径减小的能力。 导致内皮剥脱的两种损伤,气球样变和Triton治疗,在6周后导致相等的内膜增厚,尽管Triton诱导的损伤后细胞复制的短期和长期速率较低。 损伤后只有球囊扩张导致内膜平滑肌细胞慢性更新。 尽管有明显的中膜损伤,但用生理盐水过度扩张后没有新生内膜增生。 后一项研究结果表明,即使是严重的中膜损伤,在没有内皮剥脱的情况下也不会导致内膜增生。
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.