ACUTE MICROCIRCULATORY CHANGES AFTER SCALDING OF THE RAT PAW

Citation
O. Lofgren et al., ACUTE MICROCIRCULATORY CHANGES AFTER SCALDING OF THE RAT PAW, Acta Physiologica Scandinavica, 161(3), 1997, pp. 289-294
Citations number
14
Categorie Soggetti
Physiology
ISSN journal
00016772
Volume
161
Issue
3
Year of publication
1997
Pages
289 - 294
Database
ISI
SICI code
0001-6772(1997)161:3<289:AMCASO>2.0.ZU;2-0
Abstract
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.