Lowering of interstitial fluid pressure after neurogenic inflammation is inhibited by mystixin-7 peptide

Author:

Gjerde Eli-Anne B.1,Woie Kathrine1,Wei Edward T.2,Reed Rolf K.1

Affiliation:

1. Department of Physiology, University of Bergen, N-5009 Bergen, Norway; and

2. School of Public Health, University of California, Berkeley, California 94720

Abstract

Soft tissue injury is accompanied by lowering of interstitial fluid pressure (Pif), plasma protein extravasation, and edema. Inflammation was produced by electrical stimulation (ES) of the vagus and the effects of the synthetic peptide mystixin-7 ( p-anisoyl-Arg-Lys-Leu-Leu-d-Thi-Ile-d-Leu-NH2) on Pif were examined. Micropuncture measurement of Pif in submucosa, without opening the trachea, was conducted on rats anesthetized with pentobarbital sodium (50 mg/kg) and euthanized with intravenous KCl. Pif in control (intravenous saline) was −1.2 ± 0.7 mmHg before ES and decreased to −4.7 ± 1.0 mmHg ( P < 0.01, n= 8) after ES. Mystixin-7 (10 and 20 μg/kg iv) blocked the fall in Pif after ES (−1.1 ± 0.3 and −0.8 ± 0.2 mmHg, P < 0.01, n = 8 and n= 4). The 1 μg/kg dose was without effect. When trachea from animals pretreated with mystixin-7 (20 μg/kg iv) were soaked in phosphate-buffered saline (0.15 M, pH 7.4), the rate of fluid accumulation was significantly reduced. This study suggests that mystixin peptides, which have structural similarity to a fragment from laminin-α1 chain, may be useful tools for studying cell adhesion and factors that maintain the structural integrity of connective tissue after injury.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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