Karlander L E, Henriksson J, Sjöberg F
Department of Plastic Surgery, University Hospital, S-58185 Linköping, Sweden.
Microvasc Res. 2005 Jul;70(1-2):111-5. doi: 10.1016/j.mvr.2005.06.003. Epub 2005 Aug 19.
Studies using a contusion trauma model have shown that the femoral artery of the rat remains patent in 85% despite a severe vessel injury. A significant increase in tissue oxygenation (PtO2) has been found despite only a minor effect on blood flow (<20% decrease) on the muscle surface distal to the injury indicating a disturbed relationship between microvascular blood flow and metabolism. The aim of the present study was to further study the interplay between microvascular blood flow and metabolism within the distal muscle using an ethanol clearance technique (blood flow) in conjunction to the determination of an ischemia marker (lactate) by use of microdialysis. Although skeletal muscle blood flow remained unaltered as assessed by ethanol clearance, skeletal muscle lactate levels increased significantly (P<0.001) post-trauma in both legs. The increase was initially higher, faster and the increase over time larger in the trauma leg as compared to the control leg (P<0.001). These findings indicate a systemic effect of the trauma. Further, it suggests a functional impairment of the relationship between microvascular blood flow and/or muscle metabolic processes when the trauma is directed towards the supplying blood vessel. The reason for this anaerobic insult as found in this study compared to the presence of a local increase in PtO2 in the trauma leg as shown in our previous study is suggestive of an microvascular blood flow and tissue metabolism uncoupling.
使用挫伤创伤模型的研究表明,尽管大鼠股动脉受到严重血管损伤,但仍有85%保持通畅。尽管对损伤远端肌肉表面的血流影响较小(减少<20%),但已发现组织氧合(PtO2)显著增加,这表明微血管血流与代谢之间的关系受到干扰。本研究的目的是使用乙醇清除技术(血流)并结合使用微透析测定缺血标志物(乳酸),进一步研究损伤远端肌肉内微血管血流与代谢之间的相互作用。尽管通过乙醇清除评估骨骼肌血流未发生改变,但创伤后双腿骨骼肌乳酸水平均显著升高(P<0.001)。与对照腿相比,创伤腿的乳酸增加最初更高、更快,且随时间的增加更大(P<0.001)。这些发现表明创伤具有全身效应。此外,这表明当创伤针对供应血管时,微血管血流与/或肌肉代谢过程之间的关系存在功能障碍。与我们之前研究中创伤腿局部PtO2增加的情况相比,本研究中发现的这种无氧损伤的原因提示微血管血流与组织代谢解偶联。