Vol. 283, Issue 3, H933-H940, September 2002
The neurotensin fragment AcNT(8-13) inhibits
lowering of interstitial fluid pressure in rat trachea
Eli-Anne B.
Gjerde1,
Edward T.
Wei2, and
Rolf K.
Reed1
1 Department of Physiology, University of Bergen,
N-5009 Bergen, Norway; 2 School of
Public Health, University of California, Berkeley, California 94720
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.
peptide; anti-inflammatory effect; micropuncture; neurogenic
inflammation
