American Journal of Physiology - Heart and Circulatory Physiology 2002-09-01

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

Eli-Anne B Gjerde, Edward T Wei, Rolf K Reed

Index: Am. J. Physiol. Heart Circ. Physiol. 283(3) , H933-40, (2002)

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Abstract

Injury to soft tissue results in the lowering of interstitial fluid pressure (P(if)), plasma protein extravasation, and increased total tissue volume. In this study, the effects of N-acetyl neurotensin(8-13) [AcNT(8-13)] on P(if) in rat trachea were examined after electrical stimulation (ES) of the vagus nerve. P(if) was measured with glass capillaries connected to a servocontrolled counterpressure system. In pentobarbital-anesthetized female Wistar rats, the P(if) 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 microg/kg) blocked the fall in P(if) 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.