Homer-Vanniasinkam S, Rowlands T E, Hardy S C, Gough M J
Vascular Surgical Unit, The General Infirmary at Leeds, Leeds, UK.
Eur J Vasc Endovasc Surg. 2001 Dec;22(6):523-7. doi: 10.1053/ejvs.2001.1467.
Postischaemic damage in skeletal muscle may be reflected in changes to microvascular blood flow, vascular permeability, and subsequent tissue viability. Previous preclinical studies have not addressed all these parameters, and have not used periods of ischaemia and reperfusion relevant to the clinical setting. This study aimed to develop an animal model hindlimb ischaemia-reperfusion to simulate acute lower limb ischaemia.
A rodent model of hindlimb tourniquet-induced ischaemia-reperfusion was employed. Gastrocnemius muscle blood flow (GMBF; radio-labelled microspheres), oedema (GMO; using a wet:dry ratio method) and viability (GMV; histochemistry and computerised planimetry) were quantified.
6 h ischaemia per seresulted in neither muscle oedema nor loss of viability, but these changes were apparent following 4 h reperfusion. Early reperfusion at 10 min demonstrated low reflow, with GMBF improving at 120 min before declining sharply at 240 min.
Prolonged hindlimb ischaemia followed by reperfusion in this rodent model caused significant reductions in gastrocnemius muscle blood flow, associated with muscle oedema and necrosis. These three parameters have not been previously reported together in the same model. This reproducible model could be used in the evaluation of potential therapeutic intervention strategies aimed at ameliorating skeletal muscle reperfusion injury.
骨骼肌缺血后损伤可能反映在微血管血流、血管通透性及随后的组织活力变化上。以往的临床前研究并未涉及所有这些参数，且未使用与临床情况相关的缺血和再灌注时长。本研究旨在建立一种后肢缺血-再灌注动物模型以模拟急性下肢缺血。
采用啮齿动物后肢止血带诱导缺血-再灌注模型。对腓肠肌血流（GMBF；放射性标记微球法）、水肿（GMO；采用湿重：干重比法）和活力（GMV；组织化学和计算机图像分析）进行量化。
每组6小时缺血未导致肌肉水肿或活力丧失，但在4小时再灌注后这些变化明显。再灌注10分钟时早期再灌注显示低灌注，GMBF在120分钟时改善，随后在240分钟时急剧下降。
在该啮齿动物模型中，长时间后肢缺血后再灌注导致腓肠肌血流显著减少，伴有肌肉水肿和坏死。这三个参数此前未在同一模型中一起报道过。这种可重复的模型可用于评估旨在改善骨骼肌再灌注损伤的潜在治疗干预策略。
