原发性淋巴水肿患者皮肤淋巴毛细血管流速的变化。

M Fischer, U Costanzo, U Hoffmann, A Bollinger, U K Franzeck
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引用次数: 19

摘要

首次测量淋巴水肿患者皮肤微淋巴管的淋巴流速,并与健康受试者进行比较。在15名健康志愿者和16名原发性淋巴水肿患者皮下显微注射fitc -葡聚糖150,000后,采用荧光视频显微镜测量了单淋巴皮肤毛细血管的流速。原发性淋巴水肿患者淋巴毛细血管网初始充盈速度快,平均充盈速度显著高于健康对照组(890 +/- 43比550 +/- 390微米/秒,p < 0.05)。静息速度在对照组和患者之间无显著差异(10.3 +/- 4.1 vs. 16.6 +/- 13.9微米)。在16例淋巴水肿患者中,有12例观察到荧光造影剂从较深的不可见淋巴管中回流。在这些患者中,有4例患者的微淋巴管的视频密度测量显示有节律性反流的平均频率为1.4 +/- 0.5 cycles/min,其直径明显(p < 0.01)增大。预收集器的平均流速(Vp)显著高于静息流速(p < 0.01)。基于这些结果,我们提出了节律性皮肤回流起源于深层淋巴收集节的内在收缩,并通过不完善的连接通道传递到浅表微淋巴管的假设。这一新认识的机制似乎是淋巴水肿病理生理的一个重要因素。
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Flow velocity of cutaneous lymphatic capillaries in patients with primary lymphedema.

For the first time measurements of lymph flow velocities in cutaneous microlymphatics of patients with lymphedema were performed and compared with healthy subjects. Flow velocity in single lymphatic skin capillaries was measured using fluorescence video microscopy after subepidermal microinjection of FITC-dextran 150,000 in 15 healthy volunteers and 16 patients with primary lymphedema. Initial filling of the lymphatic capillary network was fast with significantly higher mean velocities in patients with primary lymphedema than in healthy controls (890 +/- 43 vs. 550 +/- 390 microns/s, p < 0.05). The resting velocities were not significantly different between controls and patients (10.3 +/- 4.1 vs. 16.6 +/- 13.9 microns). In 12 out of the 16 lymphedema patients cutaneous backflow of the fluorescent contrast medium from deeper invisible lymphatics was observed. In 4 of these patients rhythmic reflux with a mean frequency of 1.4 +/- 0.5 cycles/min was measured by video densitometry in microlymphatics with a significantly (p < 0.01) enhanced diameter. Mean flow velocity (Vp) in these precollectors was significantly increased compared to the resting velocities (p < 0.01). On the basis of these results the hypothesis is advanced that rhythmic cutaneous backflow originates from intrinsic contractions of deeper lymph collector segments and is transmitted to the superficial microlymphatics through incompetent connecting channels. This newly recognized mechanism appears to be an important factor for the pathophysiology of lymphedema.

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