Bergan John J, Pascarella Luigi, Schmid-Schönbein Geert W
Department of Surgery, University of California-San Diego, 9850 Genesee, La Jolla, CA 92037, USA.
J Vasc Surg. 2008 Jan;47(1):183-92. doi: 10.1016/j.jvs.2007.09.028.
Reflux of blood through incompetent venous valves is a major cause of the venous hypertension that underlies clinical manifestations of chronic venous disease, including varicose veins, lipodermatosclerosis, and venous ulcers.
To review published literature relating to animal models in which venous hypertension has been produced and which have yielded information on the mechanisms by which venous hypertension may trigger inflammation and cause changes in the skin and venous valves.
Medline searches, with additional papers identified from reference lists in published papers.
At least three types of animal model were identified that have contributed to a better understanding of the trigger mechanisms and role of inflammatory processes in chronic venous disease. These models involve venous hypertension induced either by acute venular occlusion, placement of a chronic arteriovenous fistula, or ligation of several large veins. Model results suggest that elevated venous pressure and altered flow can trigger inflammatory cascades in the vein wall and venous valves which can cause progressive valvular incompetence and eventual valvular destruction, and which are also important in the skin changes associated with venous disease. Treatment with agents that reduce oxidative stress by scavenging free radicals and that inhibit the inflammatory cascade can prevent the progressive deterioration of function in valves exposed to elevated venous pressure and can prevent the development of reflux blood flow.
Understanding these processes suggests potential therapeutic targets that could be effective in slowing or preventing progression, and could help promote a more positive and proactive attitude towards treatment of the underlying disease process, rather than the later manifestations of chronic venous disease.
静脉瓣膜功能不全导致的血液反流是静脉高压的主要原因，而静脉高压是慢性静脉疾病临床表现的基础，包括静脉曲张、脂肪皮肤硬化症和静脉溃疡。
综述已发表的有关动物模型的文献，这些模型产生了静脉高压，并提供了关于静脉高压可能引发炎症以及导致皮肤和静脉瓣膜变化的机制的信息。
通过医学文献数据库检索，并从已发表论文的参考文献列表中识别其他论文。
确定了至少三种动物模型，这些模型有助于更好地理解慢性静脉疾病中触发机制和炎症过程的作用。这些模型包括急性小静脉闭塞、慢性动静脉瘘的建立或多条大静脉结扎所诱导的静脉高压。模型结果表明，静脉压力升高和血流改变可触发静脉壁和静脉瓣膜中的炎症级联反应，这可导致瓣膜功能逐渐丧失和最终瓣膜破坏，并且在与静脉疾病相关的皮肤变化中也很重要。用清除自由基以降低氧化应激并抑制炎症级联反应的药物进行治疗，可以防止暴露于升高静脉压力的瓣膜功能逐渐恶化，并可以防止反流血流的发生。
了解这些过程提示了可能有效减缓或预防疾病进展的潜在治疗靶点，并有助于促进对潜在疾病过程的治疗采取更积极主动的态度，而不是仅仅针对慢性静脉疾病的后期表现。
