Department of Physiology, the Perelman School of Medicine, the University of Pennsylvania , Philadelphia, Pennsylvania.
J Appl Physiol (1985). 2018 Mar 1;124(3):761-768. doi: 10.1152/japplphysiol.00833.2017. Epub 2018 Jan 4.
Tissue P values have not been previously estimated under conditions where the blood carboxyhemoglobin % saturation ([COHb]) is at a normal level or increased. Tissue P values are not known for conditions when [COHb] is increased during CO therapy or during CO poisoning. Using a modified Krogh parallel capillary-tissue model, mean tissue P was calculated for when [COHb] was 1, 5, 10, and 15% saturation, relevant to CO therapy, and 20, 30, and 40% saturation, relevant to CO poisoning. Calculations were made for the time during which CO was being inhaled, after cessation of CO uptake, and for different O extractions from blood flowing in the model capillary. The T of relevant CO reactions was used in these calculations. When the [COHb] increased to 5 to 10% saturation, mean tissue P values increased to 500 to 1,100% of values when the [COHb] was 1% saturation. When the [COHb] increased to 20 to 40% saturation, mean tissue P values increased to 2,300 to 5,700% of the 1% saturation value. Results indicate the utility of the modified Krogh model in furthering understanding the physiology of determinants of tissue P and should facilitate future studies of in vivo CO binding to different extravascular heme proteins during CO therapy and during CO poisoning. NEW & NOTEWORTHY Tissue P levels resulting from carboxyhemoglobin concentrations achieved during CO therapy or during CO poisoning have not been previously estimated. Results published here show that at carboxyhemoglobin levels achieved during CO therapy there are 500 to 1,100% increases in mean tissue P values. With carboxyhemoglobin increases associated with toxic effects, there are 2,300 to 5,700% increases in the mean tissue P. These differences suggest a basis for understanding the therapeutic and toxic effects of CO.
组织 P 值以前未曾在血液碳氧血红蛋白饱和度([COHb])处于正常水平或升高的情况下进行估计。在 CO 治疗期间或 CO 中毒期间 [COHb] 升高时,组织 P 值未知。使用改良的 Krogh 平行毛细管组织模型,计算了当 [COHb] 饱和度分别为 1%、5%、10%和 15%(与 CO 治疗相关)以及 20%、30%和 40%(与 CO 中毒相关)时的平均组织 P 值。这些计算是在吸入 CO 的时间、停止 CO 摄取后的时间以及从流经模型毛细管的血液中不同的 O 提取进行的。这些计算使用了相关 CO 反应的 T 值。当 [COHb] 增加到 5%至 10%饱和度时,平均组织 P 值增加到 1%饱和度时的 500%至 1100%。当 [COHb] 增加到 20%至 40%饱和度时,平均组织 P 值增加到 1%饱和度时的 2300%至 5700%。结果表明,改良的 Krogh 模型在进一步了解组织 P 的决定因素的生理学方面具有实用性,并且应该有助于未来在 CO 治疗期间和 CO 中毒期间研究不同血管外血红素蛋白与 CO 的体内结合。
新的和值得注意的是,以前没有估计过在 CO 治疗期间或在 CO 中毒期间达到的碳氧血红蛋白浓度所导致的组织 P 值。这里发表的结果表明,在 CO 治疗期间达到的碳氧血红蛋白水平下,平均组织 P 值增加了 500%至 1100%。在与毒性作用相关的碳氧血红蛋白增加时,平均组织 P 值增加了 2300%至 5700%。这些差异表明了理解 CO 的治疗和毒性作用的基础。