Matsui Keiji, Ikeda Uichi, Murakami Yoshiaki, Yoshioka Toru, Shimada Kazuyuki
Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan.
Am Heart J. 2003 Feb;145(2):330-3. doi: 10.1067/mhj.2003.145.
Blood monocytes are the precursors of the lipid-laden foam cells that are the hallmark of early atherosclerotic lesions, and monocyte chemoattractant protein-1 (MCP-1) plays important roles in their recruitment to the vessel wall. In this study, we measured serum levels of MCP-1 in patients with peripheral arterial obstructive disease (PAOD) and investigated whether intravenous prostaglandin E1 (PGE1) treatment, which produces clinical benefits in PAOD, might decrease such levels.
Eight patients with PAOD at Fontaine stage II to IV were treated with a daily intravenous infusion of 10 microg of PGE1 for 7 consecutive days. Blood samples before and after 7-day PGE1 treatment were used for assays of MCP-1, interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), von Willebrand factor (vWF), and endothelin-1 (ET-1).
Serum MCP-1 levels in patients with PAOD were significantly higher than those in healthy control subjects (263.8 +/- 52.8 vs 136.5 +/- 15.0 pg/mL, P =.002). PGE1 administration for 7 days resulted in a significant decrease in the MCP-1 level, from 263.8 +/- 52.8 to 196.1 +/- 25.5 pg/mL (P =.02), whereas levels of IL-6, hs-CRP, and ET-1 and the activity of vWF were not affected.
Serum MCP-1 levels were elevated in patients with PAOD, indicating the involvement of activation of monocytes in the pathogenesis of this disorder. Parenteral administration of PGE1 appeared to decrease circulating MCP-1 levels, which might lead to the suppression of the development of atherosclerotic lesions in patients with PAOD.
血液单核细胞是富含脂质的泡沫细胞的前体,而富含脂质的泡沫细胞是早期动脉粥样硬化病变的标志,单核细胞趋化蛋白-1(MCP-1)在其募集到血管壁的过程中起重要作用。在本研究中,我们测量了外周动脉阻塞性疾病(PAOD)患者的血清MCP-1水平,并研究了在PAOD中产生临床益处的静脉注射前列腺素E1(PGE1)治疗是否可能降低此类水平。
8例Fontaine II至IV期的PAOD患者连续7天每天静脉输注10μg PGE1。7天PGE1治疗前后的血样用于检测MCP-1、白细胞介素-6(IL-6)、高敏C反应蛋白(hs-CRP)、血管性血友病因子(vWF)和内皮素-1(ET-1)。
PAOD患者的血清MCP-1水平显著高于健康对照者(263.8±52.8对136.5±15.0 pg/mL,P = 0.002)。给予PGE1 7天导致MCP-1水平显著降低,从263.8±52.8降至196.1±25.5 pg/mL(P = 0.02),而IL-6、hs-CRP和ET-1水平以及vWF活性未受影响。
PAOD患者血清MCP-1水平升高,表明单核细胞激活参与了该疾病的发病机制。胃肠外给予PGE1似乎可降低循环MCP-1水平,这可能导致PAOD患者动脉粥样硬化病变发展受到抑制。