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降低间质液压力会加重白蛋白致敏大鼠气管的水肿。

Lowering of interstitial fluid pressure will enhance edema in trachea of albumin-sensitized rats.

作者信息

Woie K, Westerberg E, Reed R K

机构信息

Department of Physiology, University of Bergen, Norway.

出版信息

Am J Respir Crit Care Med. 1996 Apr;153(4 Pt 1):1347-52. doi: 10.1164/ajrccm.153.4.8616565.

DOI:10.1164/ajrccm.153.4.8616565
PMID:8616565
Abstract

Interstitial fluid pressure (Pif) has recently been found to play an important role in edema formation in acute airway inflammation. Because airway inflammation is important in the pathogenesis of asthma, Pif was measured in rat trachea after albumin challenge to rats previously sensitized to chicken egg albumin. In pentobarbital anesthesia (50 mg/kg intraperitoneally) sensitized rats received an intravenous infusion of either saline or albumin, which circulated for 4 min. Circulatory arrest was then induced with saturated KCl intravenously to prevent further edema formation, which will increase Pif and thereby possibly cause an underestimation of an increased negativity of Pif. Pif was measured with sharpened glass capillaries (diameter 3-6 micrometer) connected to a servo-controlled counter pressure system. Pif was -1.3 +/- 0.4 mm Hg in controls and -5.8 +/- 0.5 mm Hg in sensitized rats (p < 0.01) after allergen challenge. Airway resistance was measured to verify the occurrence of airway narrowing and increased significantly in sensitized rats after allergen challenge but did not change in controls. The experimental anti-inflammatory drug, alpha-trinositol (D-myo-inositol-1,2,6-trisphosphate, 10 mg), given before or after allergen challenge abolished the increased negativity of Pif (p < 0.05), while hydrocortisone (6.25 mg) had no effect. Thus, allergen challenge is associated with a lowering of Pif, which was abolished by alpha-trinositol.

摘要

最近发现组织间隙液压力(Pif)在急性气道炎症的水肿形成中起重要作用。由于气道炎症在哮喘发病机制中很重要,因此在对先前致敏于鸡卵白蛋白的大鼠进行白蛋白激发后,测量其气管中的Pif。在戊巴比妥麻醉(腹腔注射50mg/kg)下,致敏大鼠接受静脉输注生理盐水或白蛋白,持续循环4分钟。然后静脉注射饱和氯化钾诱导循环停止,以防止进一步的水肿形成,水肿会增加Pif,从而可能导致对Pif增加的负值估计不足。使用连接到伺服控制反压系统的尖锐玻璃毛细管(直径3 - 6微米)测量Pif。变应原激发后,对照组的Pif为-1.3±0.4mmHg,致敏大鼠的Pif为-5.8±0.5mmHg(p<0.01)。测量气道阻力以验证气道狭窄的发生,变应原激发后致敏大鼠的气道阻力显著增加,而对照组未发生变化。在变应原激发之前或之后给予实验性抗炎药物α-三磷酸肌醇(D-肌醇-1,2,6-三磷酸,10mg)可消除Pif增加的负值(p<0.05),而氢化可的松(6.25mg)则无作用。因此,变应原激发与Pif降低有关,α-三磷酸肌醇可消除这种降低。

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