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淋巴微循环

Lymphatic microcirculation.

作者信息

Zawieja D C

机构信息

Department of Medical Physiology, Texas A&M University, College Station, TX 77843-1114, USA.

出版信息

Microcirculation. 1996 Jun;3(2):241-3. doi: 10.3109/10739689609148296.

DOI:10.3109/10739689609148296
PMID:8839448
Abstract

OBJECTIVE

The importance of the lymphatic system during inflammatory response is underscored by the discovery that numerous inflammatory mediators alter the lymph pump. Inhibition of the lymph pump will reduce the lymphatic outflow from the interstitial space and thus initiate the lymphatic generation of edema. We evaluated the effect that reactive oxygen metabolites have on the contractile activity of lymphatic vessels.

METHODS

Reactive oxygen metabolites are produced during inflammation and have been implicated in a number of pathologies. Exposure to reactive oxygen metabolites inhibited the lymph pump flow in a time- and concentration-dependent fashion by decreasing contraction frequency, strength, and propagation.

RESULTS

Substance P (SP) (1.0 microM) produced the following changes (% control): reductions in diastolic diameter (56%), systolic diameter (47%), and stroke volume of the lymph pump (62%); a large increase in lymphatic contraction frequency (640%); and a modest increase in lymph pump flow (43%). SP also stimulated quiescent vessels to develop typical contraction-relaxation patterns. These effects may serve to minimize the formation of edema in the face of inflammatory edemagenic conditions that are produced by SP.

CONCLUSIONS

We concluded that reactive oxygen metabolites significantly inhibit the active lymph pump and that this inhibition could be an important contributing factor in the formation of interstitial edema during inflammation We have also determined the effects of a putative mediator of inflammation (SP) on the lymphatic pumping function.

摘要

目的

众多炎症介质可改变淋巴泵,这一发现凸显了淋巴系统在炎症反应中的重要性。抑制淋巴泵会减少间质间隙的淋巴流出,从而引发淋巴性水肿。我们评估了活性氧代谢产物对淋巴管收缩活性的影响。

方法

活性氧代谢产物在炎症过程中产生,并与多种病理状况有关。暴露于活性氧代谢产物会以时间和浓度依赖的方式抑制淋巴泵流量,其机制是降低收缩频率、强度和传播。

结果

P物质(SP)(1.0微摩尔)产生了以下变化(相对于对照的百分比):舒张期直径降低(56%)、收缩期直径降低(47%)以及淋巴泵的每搏输出量降低(62%);淋巴收缩频率大幅增加(640%);淋巴泵流量适度增加(43%)。SP还刺激静止的血管产生典型的收缩 - 舒张模式。在由SP产生的炎症性致水肿情况下,这些效应可能有助于将水肿的形成降至最低。

结论

我们得出结论,活性氧代谢产物显著抑制活跃的淋巴泵,并且这种抑制可能是炎症期间间质水肿形成的一个重要促成因素。我们还确定了一种假定的炎症介质(SP)对淋巴泵功能的影响。

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