- 作者：Prabhakar Deonikar ; Mahendra Kavdia
- 刊名：Nitric Oxide
- 出版年：2013
- 出版时间：15 April, 2013
- 年：2013
- 卷：31
- 期：supp_S1
- 页码：S36-S37
- 全文大小：47 K
Background
Nitrite acts as a reservoir of nitric oxide (NO) bioactivity in the vasculature. Catalytic reduction of nitrate, diet and in vivo NO production are major sources of nitrite. Nitrite reaction with RBC-encapsulated deoxy-hemoglobin can lead to formation of NO or vasoactive species that can be further exported to cause vasodilation. Quantification of nitrite formation from NO, NO-RBC interactions metabolites and nitrite-RBC interaction metabolites is necessary to understand the nitrite reductase activity of deoxyHb.Methods
We developed an unsteady state model to quantify the formation of NO-RBC and nitrite-RBC reaction metabolites such as methemoglobin (metHb) and nitrosyl hemoglobin (HbNO) under oxygenated and deoxygenated conditions. The model geometry consists of two concentric spheres. The outer sphere represents plasma surrounding the RBC and the inner sphere represents the RBC. We estimated the concentrations of all the NO-RBC and nitrite-RBC reaction metabolites by solving the mass balance equations for each metabolite over a period of 1 min.
Results and conclusions
Using this model, we studied the effects of hematocrit and fractional oxygen saturation on NO-RBC and nitrite-RBC interactions. Our results showed that metHb, HbNO and nitrite concentrations increased with time. MetHb concentrations increased whereas HbNO and nitrite concentrations decreased with increase in fractional oxygen saturation. For a given oxygen saturation, MetHb, HbNO and nitrite increased with hematocrit. The results obtained from this model will assist in quantifying the amount and the distribution of NO or NO active species resulting from nitrite reductase activity in RBC, which can be exported to smooth muscles for vasodilation.
Disclosure
Supported by NIH Grant R01 HL084337.