J. Waller et al., A STUDY OF NEUROKININS AND OTHER EDEMA-INDUCING MEDIATORS AND MECHANISMS IN THERMAL-INJURY, Clinical and experimental pharmacology and physiology, 24(11), 1997, pp. 861-863
1. Mechanisms involved in the plasma extravasation observed following
thermal injury of rat dorsal skin were investigated. 2. Heat applied t
o the dorsal skin of anaesthetized rats by a temperature-controlled sk
in heater (1 cm diameter) for 5 min induced temperature-dependent plas
ma protein extravasation at 48-48.5 degrees C, measured for up to 4 h
following initiation of heat. 3. A tachykinin NK1 receptor antagonist
(SR140333), a bradykinin B-2 receptor antagonist (HOE140) and a cycle-
oxygenase inhibitor (indomethacin), when given as cotreatments prior t
o the selected measurement period, markedly suppressed oedema formatio
n observed over 0-1 h (P < 0.05) but not that observed over 3-4 h afte
r injury. 4. These results indicate that although neurokinins, bradyki
nin and cyclo-oxygenase products may be important for the early respon
se to thermal injury, they do not appear to play an important role in
the ongoing oedema response. 5. Neutrophils accumulate at the inflamma
tory site by 4 h after thermal injury, Therefore, the effect of deplet
ion of circulating neutrophils by a rat anti-neutrophil antiserum on o
edema formation over the 0-4 h period was investigated, The results sh
ow that oedema formation was similar in control and antineutrophil-tre
ated rats. 6. In conclusion, the data from the present study indicate
that neuropeptides as well as other vasoactive mediators play a role i
n the acute plasma extravasation observed after thermal injury, but no
t in the ongoing inflammatory injury, Neutrophils, despite their prese
nce at sites of thermal injury, do not appear to be involved in mediat
ing the oedema formation observed up to 4 h after thermal injury.