Nitrite anion stimulates ischemic arteriogenesis involving NO metabolism
Nitrite anion stimulates ischemic arteriogenesis involving NO metabolism
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DOI：
10.1152/ajpheart.01086.2010
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发表时间：
2012-07-01
影响因子：
4.8
通讯作者：
Kevil, Christopher G.
中科院分区：
文献类型：
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作者：
Bir, Shyamal C.;Pattillo, Christopher B.;Kevil, Christopher G.
Bir SC，Pattillo CB，Pardue S，Kolluru GK，Docherty J，Goyette D，Dvorsky P，Kevil CG.亚硝酸根阴离子刺激缺血性动脉生成，涉及NO代谢。Am J Physiol Heart Circ Physiol 303：H178-H188，2012。首次发表于2012年5月18日; doi：10.1152/ajpheart.01086.2010.-一氧化氮（NO）是缺血性血管重塑的潜在调节剂，因此增加其生物利用度的疗法可用于治疗缺血性组织疾病。在这里，我们研究了在建立的组织缺血期间，施用NO前药亚硝酸钠对动脉生成活性的影响。采用永久性单侧股动静脉结扎法制备慢性后肢缺血模型。结扎后5天，将动物随机分配至对照PBS或亚硝酸钠（165 μ g/kg）治疗组，每日两次。使用SPY血管造影术和Microfil血管铸型纵向测量原位血管重塑。延迟亚硝酸钠治疗迅速增加缺血肢体动脉血管直径和分支的NO依赖性的方式。SPY成像血管造影显示，亚硝酸盐治疗增强了从股深到隐动脉的缺血性股薄肌侧支血管形成。平滑肌细胞肌动蛋白的免疫荧光染色也证实，亚硝酸钠治疗增加动脉生成的NO依赖的方式。NO前药亚硝酸钠显著增加已建立的严重慢性组织缺血的动脉生成和再灌注。
Bir SC, Pattillo CB, Pardue S, Kolluru GK, Docherty J, Goyette D, Dvorsky P, Kevil CG. Nitrite anion stimulates ischemic arteriogenesis involving NO metabolism. Am J Physiol Heart Circ Physiol 303: H178-H188, 2012. First published May 18, 2012; doi:10.1152/ajpheart.01086.2010.-Nitric oxide (NO) is a potential regulator of ischemic vascular remodeling, and as such therapies augmenting its bioavailability may be useful for the treatment of ischemic tissue diseases. Here we examine the effect of administering the NO prodrug sodium nitrite on arteriogenesis activity during established tissue ischemia. Chronic hindlimb ischemia was induced by permanent unilateral femoral artery and vein ligation. Five days postligation; animals were randomized to control PBS or sodium nitrite (165 mu g/kg) therapy twice daily. In situ vascular remodeling was measured longitudinally using SPY angiography and Microfil vascular casting. Delayed sodium nitrite therapy rapidly increased ischemic limb arterial vessel diameter and branching in a NO-dependent manner. SPY imaging angiography over time showed that nitrite therapy enhanced ischemic gracillis collateral vessel formation from the profunda femoris to the saphenous artery. Immunofluorescent staining of smooth muscle cell actin also confirmed that sodium nitrite therapy increased arteriogenesis in a NO-dependent manner. The NO prodrug sodium nitrite significantly increases arteriogenesis and reperfusion of established severe chronic tissue ischemia.