Löfgren O, Gazelius B, Lundeberg T
Department of Physiology and Pharmacology, Karolinska Institutet, Sweden.
Acta Physiol Scand. 1997 Nov;161(3):289-94. doi: 10.1046/j.1365-201X.1997.00219.x.
A scalding model in the anaesthetized rat was used to measure acute circulatory reactions after heat exposure. Local blood flow of both hindpaws was recorded simultaneously and continuously by laser Doppler flowmetry before, during and for 2 hours following scalding. The scalding injury was inflicted by dipping the right hindpaw into hot water at 60 degrees C for 20 s. Concomitantly, the mean arterial blood pressure (MAP) was displayed on a chart recorder. MAP was obtained by cannulation of the common carotid artery. Oedema formation was calculated by measuring the volume changes of the hindpaws in a plethysmometer before and 30, 60 and 120 min after scalding. Scalding was followed by a biphasic increase of cutaneous circulation. During the first minute after heat provocation, an immediate increase in blood perfusion of about 400% was recorded, followed by a slow decrease of circulation. At 30 min after scalding, there was a secondary phase of increased microcirculation of approximately 230%. A slow decline of cutaneous circulation then followed, and after about 60 min the value was stabilized at approximately 100% above pre-burn level throughout the observation time. Almost no change of perfusion was observed on the contralateral unscalded paw. The scalding injury was followed by a progressive oedema formation on the scalded paw, measured by a volume increase of approximately 72% during the observation period, whereas the non-scalded paw showed no change. MAP remained at a stable level throughout the experiment except for a short-lasting transient increase of approximately 10% at the same time as the first peak of blood perfusion. We could thus confirm that scalding in the present model is accompanied by an immediate and marked increase in the peripheral circulation of the scalded paw followed by a later propagation of oedema, and that these inflammatory changes do not appear to be related to central haemodynamic alterations.
采用麻醉大鼠烫伤模型来测量热暴露后的急性循环反应。在烫伤前、烫伤期间及烫伤后2小时,通过激光多普勒血流仪同时连续记录双侧后爪的局部血流。将右后爪浸入60摄氏度的热水中20秒造成烫伤。同时,平均动脉血压(MAP)在图表记录器上显示。通过颈总动脉插管获取MAP。通过在体积描记器中测量烫伤前及烫伤后30、60和120分钟后后爪的体积变化来计算水肿形成情况。烫伤后皮肤循环呈双相增加。在热刺激后的第一分钟,记录到血液灌注立即增加约400%,随后循环缓慢下降。烫伤后30分钟,出现微循环增加的第二阶段,约为230%。随后皮肤循环缓慢下降,约60分钟后,在整个观察期内该值稳定在高于烫伤前水平约100%。在对侧未烫伤的爪子上几乎未观察到灌注变化。烫伤后,烫伤爪上出现渐进性水肿形成,在观察期内体积增加约72%,而未烫伤的爪子无变化。除了在血液灌注的第一个峰值出现的同时MAP有短暂约10%的短暂增加外,MAP在整个实验过程中保持稳定水平。因此我们可以证实,在本模型中,烫伤伴随着烫伤爪外周循环立即且显著增加,随后出现水肿扩散,并且这些炎症变化似乎与中心血流动力学改变无关。