Department of Neurosurgery, Neuroscience Research Center, Kerman, Iran.
Spine (Phila Pa 1976). 2011 Oct 15;36(22):1824-8. doi: 10.1097/BRS.0b013e3181d4e15a.
An experimental study to measure the depth of penetration of new vessels in degenerated intervertebral disc in rat.
To evaluate the effects of atorvastatin on angiogenesis in experimental disc degeneration in rat.
Back pain is strongly associated with degenerated intervertebral disc and management of this condition is still empirical. Decrease of nucleus nutrition due to loss of vascularity with aging may aggravate the process of disc degeneration. So, angiogenesis may be useful in the healing process of degenerated disc. In this study, we wanted to evaluate the effect of atorvastatin, whose stimulating effect on angiogenesis on other tissues was shown in several studies, on degenerated intervertebral disc in rat.
Atorvastatin was administered intraperitoneally for 6 weeks in doses of 1, 4, and 8 mg/kg in rats after experimental disc degeneration. The rats intervertebral disc sections were stained immunohistochemically for von Willebrand Factor to evaluate the depth of vessels penetration and degree of vascularity.
In the nonoperated control group, the intervertebral discs were avascular. But experimental disc degeneration promoted angiogenesis. In this group, the mean of penetration was 49.25 μ (standard deviation = 19.905). Atorvastatin stimulated angiogenesis after experimental disc degeneration in the rats and the angiogenesis was more significant in the high and medium dose groups than operated control group. High-dose atorvastatin could not inhibit angiogenesis in experimental degenerated disc. There was no any significant difference in degree of vascularity among the groups.
Atorvastatin stimulates angiogenesis in experimental disc degeneration in rats. But, it does not show a biphasic effect.
一项旨在测量大鼠退变椎间盘中新血管穿透深度的实验研究。
评估阿托伐他汀对大鼠实验性椎间盘退变中血管生成的影响。
腰痛与退变椎间盘密切相关，其治疗仍处于经验阶段。随着年龄的增长，血管减少导致核营养减少，可能会加重椎间盘退变过程。因此，血管生成可能对退变椎间盘的愈合过程有用。在这项研究中，我们希望评估阿托伐他汀对大鼠退变椎间盘的作用，因为已有研究表明阿托伐他汀对其他组织有促进血管生成的作用。
在大鼠实验性椎间盘退变后，阿托伐他汀以 1、4 和 8mg/kg 的剂量腹腔内给药 6 周。用免疫组织化学法对 von Willebrand 因子进行染色，评估血管穿透深度和血管密度。
在未手术对照组中，椎间盘无血管。但实验性椎间盘退变促进了血管生成。在该组中，平均穿透深度为 49.25μ（标准差=19.905）。阿托伐他汀在大鼠实验性椎间盘退变后刺激血管生成，高、中剂量组的血管生成比手术对照组更为显著。高剂量阿托伐他汀不能抑制实验性退变椎间盘的血管生成。各组的血管密度无显著差异。
阿托伐他汀可刺激大鼠实验性椎间盘退变中的血管生成，但无双相作用。
