Schwab S, Spranger M, Krempien S, Hacke W, Bettendorf M
Department of Neurology, University of Heidelberg, Germany.
Stroke. 1997 Sep;28(9):1744-8. doi: 10.1161/01.str.28.9.1744.
The insulin-like growth factors (IGF) are synthesized in the brain and are involved in fetal brain development. An increased expression of IGF-I and IGF-II occurs in cerebral regions with neuronal damage after experimental hypoxic injury. Furthermore, the expression of mRNAs coding for IGF-I and the binding proteins IGFBP-2 and IGFBP-3 is augmented in response to unilateral ischemia in animal models. The secretory dynamics of IGF-I in human cerebral ischemia have not yet been investigated.
Plasma IGF-I and IGFBP-3 were measured sequentially in 20 patients with acute ischemic stroke (within 24 hours and 3, 5, and 10 days thereafter). For analysis the patients were assigned to three groups according to the diameter of the infarct area as measured on CT scan: small (< 1.5 cm), moderate (> or = 1.5 cm and < or = 5 cm), and large (> 5 cm). Eight age-matched patients with nonvascular, neurological illnesses served as controls.
Plasma IGF-I and IGFBP-3 plasma concentrations after acute cerebral ischemia were strikingly lower than those in control subjects and healthy individuals reported in the literature. Plasma IGF-I levels in patients with large infarcts were significantly statistically lower than those in control subjects (P < .05), and plasma IGFBP-3 levels were significantly lower than those in control subjects on days 5 and 10.
IGF-I and IGFBP-3 plasma levels are decreased in patients after cerebral ischemia. After acute ischemic stroke, increased demand for growth factors, altered tissue distribution, and accelerated metabolic clearance rate or central inhibition of the somatotrophic axis may contribute to these low plasma concentrations. Growth factors such as IGF-I and IGFBP-3 may play an important role in the pathophysiology of acute cerebral ischemia, and growth factors may have a considerable effect on future therapeutic regimens.
胰岛素样生长因子（IGF）在脑内合成，参与胎儿脑发育。实验性缺氧损伤后，IGF-I和IGF-II在神经元损伤的脑区表达增加。此外，在动物模型中，单侧缺血后编码IGF-I及结合蛋白IGFBP-2和IGFBP-3的mRNA表达增强。但尚未对人脑缺血时IGF-I的分泌动力学进行研究。
对20例急性缺血性卒中患者（发病24小时内及之后3、5和10天）连续测定血浆IGF-I和IGFBP-3。根据CT扫描测量的梗死面积直径将患者分为三组：小面积梗死（<1.5 cm）、中等面积梗死（≥1.5 cm且≤5 cm）和大面积梗死（>5 cm）。8例年龄匹配的非血管性神经系统疾病患者作为对照。
急性脑缺血后患者血浆IGF-I和IGFBP-3浓度显著低于文献报道的对照受试者和健康个体。大面积梗死患者的血浆IGF-I水平显著低于对照受试者（P<0.05），血浆IGFBP-3水平在第5天和第10天时显著低于对照受试者。
脑缺血患者血浆IGF-I和IGFBP-3水平降低。急性缺血性卒中后，生长因子需求增加、组织分布改变、代谢清除率加快或生长激素轴的中枢抑制可能导致这些血浆浓度降低。IGF-I和IGFBP-3等生长因子可能在急性脑缺血的病理生理学中起重要作用，且生长因子可能对未来治疗方案有显著影响。
