建立大鼠急性和慢性后肢缺血模型,研究两组大鼠病变特点及缺血代偿情况。

选择3月龄成年、高脂血症SD大鼠建立急性(n = 20)和慢性(n = 20)后肢缺血模型。采用实时荧光定量PCR和2^-△△Ct法,检测股动脉闭塞后6 h患肢股内收肌血管内皮生长因子(VEGF)和缺氧诱导因子(HIF-1α)的相对定量。股动脉闭塞1周后取腓肠肌检查组织坏死及炎症浸润情况。股动脉闭塞后4周后采用免疫组织化学染色法计算股内收肌毛细血管/肌纤维比例。术后记录患肢运动功能及患肢/健肢股骨中段周径比值。

急性组大鼠术后即刻表现严重肢体缺血。慢性组平均术后(8.2 ± 0.7)d始表现严重肢体缺血。股动脉闭塞后6 h,急性组股内收肌目标基因VEGF和HIF-1α的相对定量均高于慢性缺血组[(5.57 ± 0.87) vs. (2.49 ± 0.85)和(10.28 ± 1.09) vs. (6.83 ± 1.17),P < 0.05]。股动脉闭塞后1周,急性组腓肠肌病理组织学检查显示较多坏死及炎症浸润。股动脉闭塞后4周,急性组股内收肌毛细血管/肌纤维比例显著高于慢性组[(1.37 ± 0.14) vs. (1.18 ± 0.12),P < 0.05]。缺血肢体功能评分结果显示,急性缺血肢体运动功能早期受损甚于慢性组(P < 0.05),但后期恢复较优(P均< 0.05)。

急、慢性缺血具有不同的病理损伤特点,进而表现出不同的缺血代偿机制。急性大鼠缺血的代偿优于慢性缺血。

To study the different ischemic characteristics and compensatory mechanisms of acute or chronic rats hindlimb ischemia.

Three months SD rats with hyperlipemia were used to induce the acute (n = 20) or chronic (n = 20) hindlimb ischemia. Real-time PCR and 2-^△△CT Methods were used to analyze VEGF and HIF-1α in adductor femoris tissue at 6h after femoral artery (FA) occlusion in both groups. Muscle necrosis and inflammation in gastrocnemius were observed at 1 week after FA occlusion. Four weeks after FA occlusion, the ratio of capillary to fibromuscular in ischemic adductorfemoris were counted after immunohistochemical stain. Capability of movement and diameter for ischemic limbs were recorded weekly postoperation.

Acute group showed critical limb ischemia immediately after operation, but Chronic group expressed it at (8.2 ± 0.7) days postsurgical. At 6 h after FA occlusion, the relative quantity of VEGF and HIF-1α were significantly higher than chronic group [(5.57 ± 0.87) vs. (2.49 ± 0.85) and (10.28 ± 1.09) vs. (6.83 ± 1.17), P < 0.05]. At 1 week, acute ischemic gastrocnemius showed more muscle necrosis and inflammation. At 4 week, the ratio of capillary/fibromuscular in acute ischemic adductorfemoris significantly increased than chronic group [(1.37 ± 0.14) vs. (1.18 ± 0.12), P < 0.05]. The acute ischemic limb dysfunction were more severe early after surgical, however, it recovered better at 3 or 4 week postsurgical.

Pathological feature induced by acute or gradual ischemia are different, which cause different compensatory response to ischemia injury. Rats show the better compensation to acute ischemia than to chronic ischemia.