Study on Oxidation Stability and Oxygen Affinity of Hemoglobin During Storage

2018 ◽  
Vol 42 (12) ◽  
pp. 1185-1195 ◽  
Author(s):  
Qiuhui Li ◽  
Huiya Ma ◽  
Yuanyuan Zhang ◽  
Kun Feng ◽  
Hongli Zhu ◽  
...  
Keyword(s):  
Oxidation Stability ◽  
Oxygen Affinity ◽  
Oxygen Affinity Of Hemoglobin

scholarly journals GBT1118, a compound that increases the oxygen affinity of hemoglobin, improves survival in murine hypoxic acute lung injury

2018 ◽  
Vol 124 (4) ◽  
pp. 899-905 ◽  
Author(s):  
Nathan D. Putz ◽  
Ciara M. Shaver ◽  
Kobina Dufu ◽  
Chien-Ming Li ◽  
Qing Xu ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Oxygen Affinity ◽  
High Dose ◽  
Novel Therapy ◽  
Oxygen Affinity Of Hemoglobin

Acute respiratory distress syndrome (ARDS) is characterized by lung inflammation and pulmonary edema, leading to arterial hypoxemia and death if the hypoxemia is severe. Strategies to correct hypoxemia have the potential to improve clinical outcomes in ARDS. The goal of this study was to evaluate the potential of hemoglobin modification as a novel therapy for ARDS-induced hypoxemia. The therapeutic effect of two different doses of GBT1118, a compound that increases the oxygen affinity of hemoglobin, was evaluated in a murine model of acute lung injury induced by intratracheal LPS instillation 24 h before exposure to 5% or 10% hypoxia ( n = 8–15 per group). As expected, administration of GBT1118 to mice significantly increased the oxygen affinity of hemoglobin. Compared with mice receiving vehicle control, mice treated with GBT1118 had significantly lower mortality after LPS + 5% hypoxia (47% with vehicle vs. 22% with low-dose GBT1118, 13% with high-dose GBT1118, P = 0.032 by log rank) and had reduced severity of illness. Mice treated with GBT1118 showed a sustained significant increase in SpO2 over 4 h of hypoxia exposure. Treatment with GBT1118 did not alter alveolar-capillary permeability, bronchoalveolar lavage (BAL) inflammatory cell counts, or BAL concentrations of IL-1β, TNF-α, or macrophage inflammatory protein-1α. High-dose GBT1118 did not affect histological lung injury but did decrease tissue hypoxia as measured intensity of pimonidazole (Hypoxyprobe) staining in liver ( P = 0.043) and kidney ( P = 0.043). We concluded that increasing the oxygen affinity of hemoglobin using GBT1118 may be a novel therapy for treating hypoxemia associated with acute lung injury. NEW & NOTEWORTHY In this study, we show that GBT1118, a compound that increases hemoglobin affinity for oxygen, improves survival and oxygen saturation in a two-hit lung injury model of intratracheal LPS without causing tissue hypoxia. Modulation of hemoglobin oxygen affinity represents a novel therapeutic approach to treatment of acute lung injury and acute respiratory distress syndrome, conditions characterized by hypoxemia.

A Comparison of Diphosphonoglyceric Acid and Diphosphoglyceric Acid as Allosteric Effectors for Hemoglobin

1973 ◽  
Vol 51 (7) ◽  
pp. 1120-1122 ◽  
Author(s):  
Ruth E. Benesch ◽  
Reinhold Benesch ◽  
Suzanna Yung ◽  
Erich Baer ◽  
Ranga Robinson
Keyword(s):  
Binding Site ◽  
Oxygen Affinity ◽  
Glyceric Acid ◽  
Oxygen Release ◽  
Allosteric Effectors ◽  
Oxygen Affinity Of Hemoglobin

2,3-Diphosphoglycerate is the major intraerythrocytic cofactor for oxygen release by hemoglobin. The phosphono analogue, 2,3-diphosphono-DL-glyceric acid, has only minimal effects on the oxygen affinity of hemoglobin. This finding is readily understood in terms of the electrostatic and spatial requirements of the binding site in deoxyhemoglobin.

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