Modeling O₂-dependent effects of nitrite reductase activity in blood and tissue on coupled NO and O₂ transport around arterioles.

Modeling O₂-dependent effects of nitrite reductase activity in blood and tissue on coupled NO and O₂ transport around arterioles.
复制标题

模拟血液和组织中亚硝酸还原酶活性对小动脉周围 NO 和 O 转运耦合的 O 依赖性影响。

DOI:
10.1007/978-1-4419-7756-4_36
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发表时间:
2011
影响因子:
--
通讯作者:
Jaron,Dov
Jaron,Dov
中科院分区:
医学4区
文献类型:
--
作者:
Buerk,DonaldG;Barbee,KennethA;Jaron,Dov

文献摘要

相似文献

文献中最近的证据表明,在缺血或缺氧条件下,组织在将亚硝酸盐还原为NO方面比血液发挥更大的作用。我们以前的数学模型耦合NO和O2运输周围的小动脉,修改,包括超氧化物生成功能障碍的内皮细胞,进一步发展,包括亚硝酸盐还原酶活性在血液和组织。稳态径向和轴向的NO和PO2在小动脉和周围组织的配置文件进行了模拟不同的血液流速和动脉血PO2值。由此产生的计算机模拟表明,血液中的亚硝酸盐还原酶活性是不是一个非常有效的机制,保存NO由于强大的清除NO的血红蛋白。相比之下,组织中的亚硝酸还原酶活性在增加血管壁中的NO生物利用度方面更有效,并且随着组织缺氧变得更严重,逐渐贡献更多的NO。
Recent evidence in the literature suggests that tissues play a greater role than blood in reducing nitrite to NO under ischemic or hypoxic conditions. Our previous mathematical model for coupled NO and O2transport around an arteriole, modified to include superoxide generation from dysfunctional endothelium, was developed further to include nitrite reductase activity in blood and tissue. Steady-state radial and axial NO and pO2profiles in the arteriole and surrounding tissue were simulated for different blood flow rates and arterial blood pO2values. The resulting computer simulations demonstrate that nitrite reductase activity in blood is not a very effective mechanism for conserving NO due to the strong scavenging of NO by hemoglobin. In contrast, nitrite reductase activity in tissue is much more effective in increasing NO bioavailability in the vascular wall and contributes progressively more NO as tissue hypoxia becomes more severe.