The neurotensin fragment AcNT(8–13) inhibits lowering of interstitial fluid pressure in rat trachea

Abstract

Injury to soft tissue results in the lowering of interstitial fluid pressure (Pif), plasma protein extravasation, and increased total tissue volume. In this study, the effects of N-acetyl neurotensin(8–13) [AcNT(8–13)] on Pif in rat trachea were examined after electrical stimulation (ES) of the vagus nerve. Pif was measured with glass capillaries connected to a servocontrolled counterpressure system. In pentobarbital-anesthetized female Wistar rats, the Pif after intravenous saline was −1.8 ± 0.3 mmHg (means ± SD) and decreased to −5.0 ± 0.6 mmHg ( P < 0.01, n = 9) after ES. AcNT(8–13) (10 μg/kg) blocked the fall in Pif after ES (−2.5 ± 2.3 mmHg, P < 0.01, n = 8). In tracheal tissue from animals pretreated with AcNT(8–13) at the same dose and immersed in phosphate-buffered saline (0.15 M, pH 7.4), the rate of fluid accumulation in excised tissues was significantly reduced after 2 h. The ability of AcNT(8–13) to modulate the fluid mechanics of tracheal interstitium after inflammation suggests that it may be a useful tool for studying cell adhesion and related factors that maintain structural integrity of connective tissue after injury.