Changes in Plasma Levels of Oxygen Radical Scavenging Enzymes during Extracorporeal Membrane Oxygenation in a Lamb Model

Evidence in the literature has generally supported either of two paraquat resistance mechanisms: an increase in activity of oxygen radical-scavenging enzymes in resistant plants which affords protection from active oxygen species formed by paraquat; and sequestration of paraquat away from its site of action in the chloroplast. Evidence for the first model relies primarily on measurement of increased enzyme activity and cross-resistance to other oxygen radical-generating stresses in resistant plants. The sequestration model is supported by data showing decreased translocation of paraquat and absence of paraquat injury in plant systems that do not have increased levels of protective enzymes. An alteration in paraquat transport at one of several plant cell membranes could confer resistance by modifying movement of paraquat into the compartment bounded by that membrane. Properties of the plasmalemma, chloroplast envelope, and tonoplast that may be important to paraquat transport are discussed and data supporting or discounting specific membrane alterations in resistant plants are presented. Finally, the possibility that both mechanisms may work in concert is addressed.

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Changes in the Levels of Beta-thromboglobulin and Inflammatory Mediators during Extracorporeal Membrane Oxygenation Support

The International Journal of Artificial Organs ◽

10.5301/ijao.5000617 ◽

2017 ◽

Vol 40 (10) ◽

pp. 575-580 ◽

Cited By ~ 8

Author(s):

Jae H. Chung ◽

Hye J. Yeo ◽

Dohyung Kim ◽

Sun M. Lee ◽

Junhee Han ◽

...

Keyword(s):

Respiratory Failure ◽

Extracorporeal Membrane Oxygenation ◽

Acute Respiratory Failure ◽

Platelet Activation ◽

Plasma Levels ◽

Statistical Significance ◽

Early Period ◽

Platelet Dysfunction ◽

Platelet Factor ◽

Membrane Oxygenation

Background Extracorporeal membrane oxygenation (ECMO) has been associated with platelet dysfunction, but no markers of platelet dysfunction during ECMO have been identified. Methods We investigated the potential uses of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) as markers of platelet activation induced by ECMO in vivo. Results 13 patients who received ECMO for acute respiratory failure were included. Generalized estimating equations were used to examine the associations between days on ECMO and the plasma levels of beta-TG and PF4 and of proinflammatory markers. Analyses were performed before ECMO (baseline) and 24, 48, 72 and 168 hours after the commencement of ECMO. The plasma levels of biomolecules were measured by ELISA and Luminex assay. Percentages of platelets varied widely without statistical significance (p = 0.17). Beta-TG levels significantly decreased over the first 72 hours (p<0.001), but PF4 levels decreased nonsignificantly (p = 0.17). Inflammatory markers, that is, plasma IL-6 (p = 0.03), IL-18 (p<0.001), and MMP-8 (p<0.01) levels stabilized during an early period of ECMO support. Conclusions Our data suggest that ECMO use may not affect platelet activation during the first 3 days of ECMO. Plasma beta-TG levels may allow assessment of the time-dependent extent of ECMO-induced platelet dysfunction in patients with acute respiratory failure.

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