A scalding model in the anaesthetized rat was used to measure acute ci
rculatory reactions after heal exposure. Local blood flow of both hind
paws was recorded simultaneously and continuously by laser Doppler flo
wmetry before, during and for 2 hours following scalding. The scalding
injury was inflicted by dipping the right hindpaw into hot water at 6
0 degrees C: for 20 c. Concomitantly, the mean arterial blood pressure
(MAP) was displayed on a chart recorder. MAP was obtained by cannulat
ion of the common carotid artery. Oedema formation was calculated by m
easuring the volume changes of the hindpaws in a plethysmometer before
and 30, 60 ard 120 min after scalding. Scalding was followed by a bip
hasic increase of cutaneous circulation. During the first minute after
heat provocation, an immediate increase in blood perfusion of about 4
00% was recorded, followed by a slow decrease of circulation, At 30 mi
n after scalding, there was a secondary phase of increased microcircul
ation of approximatelly 230%. A slow decline of cutaneous circulation
then followed, and after about 60 min the value was stabilized at appr
oximate to 100% above pre-burn level throughout the observation time.
Almost no change of perfusion was observed on the contralateral unscal
ded paw. The scalding injury was followed by a progressive oedema form
ation on the scalded paw, measured by a volume increase of approximate
to 72% during the observation period, whereas the non-scalded paw sho
wed no change. MAP remained at a stable level throughout the experimen
t except for a short-lasting transient increase of approximate to 10%
at the same time as the first peak of blood perfusion. We could thus c
onfirm that scalding in the present model is accompanied by an immedia
te and marked increase in the peripheral circulation of the scalded pa
w followed by a later propagation oi oedema, and that these inflammato
ry changes do not appear to be related to central haemodynamic alterat
ions.