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慢性静脉功能不全中的炎症。这个问题无法克服吗?

Inflammation in chronic venous insufficiency. Is the problem insurmountable?

作者信息

Takase S, Delano F A, Lerond L, Bergan J J, Schmid-Schönbein G W

机构信息

Department of Bioengineering and Institute for Biomedical Engineering, University of California, San Diego, Calif., USA.

出版信息

J Vasc Res. 1999;36 Suppl 1:3-10. doi: 10.1159/000054068.

DOI:10.1159/000054068
PMID:10474045
Abstract

One of the hallmarks of venous insufficiency is an elevated venous pressure. While a number of mechanisms have been proposed for vascular and parenchymal cell damage following venous pressure elevation, such as white cell infiltration, a key question remains as to what degree venous occlusion and flow interruption per se may constitute a risk factor in venous disease. To gain an insight into this mechanism, we examined the effect of venous occlusion followed by reperfusion. A draining venule (circa 50 micrometer) in the rat mesentery was occluded with a micropipette (1 h) followed by reperfusion (1 h). The procedure serves to raise the microvascular pressure to about 31 mm Hg during the occlusion while the flow is completely stopped in the local venous and capillary network. Parenchymal cell death in the mesentery was monitored by propidium iodide (PI) labeling. The number of PI-positive cells significantly increased predominantly during reperfusion. A 1-week treatment with a micronized purified flavonoid fraction (100 mg/kg/day) served to significantly reduce parenchymal cell death as well as leukocyte rolling, adhesion to postcapillary venule, and migration into the tissue both during occlusion and reperfusion. The results indicate, that even in an initially symptomless tissue, flow reduction combined with microvascular pressure elevation during venous occlusion results in tissue damage not only during reperfusion (as in arterial occlusion) but also during occlusion.

摘要

静脉功能不全的一个标志是静脉压升高。虽然已经提出了许多关于静脉压升高后血管和实质细胞损伤的机制,如白细胞浸润,但一个关键问题仍然存在,即静脉阻塞和血流中断本身在多大程度上可能构成静脉疾病的危险因素。为了深入了解这一机制,我们研究了静脉阻塞后再灌注的影响。用微量移液器阻塞大鼠肠系膜中的一条引流小静脉(约50微米)1小时,然后再灌注1小时。该操作在阻塞期间可将微血管压力提高到约31毫米汞柱,而局部静脉和毛细血管网络中的血流则完全停止。通过碘化丙啶(PI)标记监测肠系膜中的实质细胞死亡。PI阳性细胞的数量主要在再灌注期间显著增加。用微粉化纯化类黄酮组分(100毫克/千克/天)进行为期1周的治疗,可显著减少实质细胞死亡以及白细胞滚动、对毛细血管后小静脉的黏附以及在阻塞和再灌注期间向组织内的迁移。结果表明,即使在最初无症状的组织中,静脉阻塞期间血流减少与微血管压力升高不仅会在再灌注期间(如动脉阻塞时)导致组织损伤,而且在阻塞期间也会导致组织损伤。

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