The Incidence of Decreased Red Blood Cell Deformability in Sepsis and the Association With Oxygen Free Radical Damage and Multiple-System Organ Failure

Machiedo, George W.

doi:10.1001/archsurg.1989.01410120032007

Cited by 108 publications

(65 citation statements)

References 14 publications

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“…Although this study could not determine the source(s) of catalytic iron, we found a significant association between plasma catalytic iron and free hemoglobin levels, suggesting that free hemoglobin from ex vivo hemolysis (e.g., pRBC transfusions) and/or in vivo hemolysis (e.g., sepsis) (31,32) are potentially relevant sources. Supporting this notion, we found a significant dose-response relation between pRBC transfusions before ICU arrival and plasma catalytic iron levels on ICU day 1.…”

Section: Discussionmentioning

confidence: 60%

Plasma Catalytic Iron, AKI, and Death among Critically Ill Patients

Leaf

Rajapurkar²,

Lele

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Catalytic iron has been hypothesized to be a key mediator of AKI. However, the association between plasma catalytic iron levels and AKI has not been well studied in humans.Design, settings, participants, & measurements A single-center, prospective, nonconsecutive cohort study of 121 critically ill patients admitted to intensive care units (ICUs) between 2008 and 2012 was performed. Plasma catalytic iron, free hemoglobin, and other iron markers were measured on ICU days 1 and 4. The primary end point was in-hospital mortality or AKI requiring RRT. Secondary end points included mortality (assessed during hospitalization, at 30 days, and 1 year) and incident AKI, defined by modified Kidney Disease Improving Global Outcomes criteria.Results ICU day 1 plasma catalytic iron levels were higher among patients who reached the primary end point (median, 0.74 mmol/l [interquartile range, 0.31-3.65] versus 0.29 mmol/l [0.22-0.46]; P,0.01). ICU day 1 plasma catalytic iron levels were associated with number of packed red blood cell transfusions before ICU arrival (r s =0.29; P,0.001) and plasma free hemoglobin levels on ICU day 1 (r s =0.32; P,0.001). Plasma catalytic iron levels on ICU day 1 were significantly associated with in-hospital mortality or AKI requiring RRT, even after adjusting for age, enrollment eGFR, and number of packed red blood cell transfusions before ICU arrival (13 events; adjusted odds ratio per 1-SD higher ln[catalytic iron], 3.33; 95% confidence interval, 1.79 to 6.20). ICU day 1 plasma catalytic iron levels were also significantly associated with incident AKI, RRT, hospital mortality, and 30-day mortality.Conclusions Among critically ill patients, elevated plasma catalytic iron levels on arrival to the ICU are associated with a greater risk of incident AKI, RRT, and hospital mortality.

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Section: Discussionmentioning

confidence: 60%

Plasma Catalytic Iron, AKI, and Death among Critically Ill Patients

Leaf

Rajapurkar²,

Lele

et al. 2014

Clinical Journal of the American Society of Nephrology

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“…The more compact the diameter on the OSCPs (50 nm) is, the more often the influence of it's to cells and the molecular effects of it's about the intracellular systems increases. Earlier scientific studies, demonstrated that reactive oxygen species (ROS) caused by nanoparticles are able to bring about damage of red blood cells [14,15] and also the information exhibited various consequences based on switches within the diameter of nanoparticles, the distribution of theirs in the route and body tissues of consumption as well as time period of exposure. Actually ROS through the of OSCPs have assaulted hepatocytes and also available ALT kept in them putting in into the blood serum; whereas; the immune effect of mice to an outside element continues to be the expansion on the variety of white blood cells for phagocytosis of Nanosilver particles [16].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Induced by Organo Sliver Clay Particles in Mice

2017

IJSR

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“…The first mechanism is thought to be mediated by free radical-induced deformities of the RBCs. 18 The cellular defect in the ability to utilize O 2 is possibly aggravated by the increased PCOOH, which may render hepatocytes less able to accept and utilize O 2 , causing a significant fall in ATP and EC. α-Tocopherol was found to be significantly low in model 3 after 24 h (P Ͻ 0.001).…”

Section: Discussionmentioning

confidence: 99%

Hepatic phosphatidylcholine hydroperoxide content in noncirrhotic, cirrhotic, and antioxidant-treated rats with endotoxemia

et al. 1999

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Hepatic phosphatidylcholine hydroperoxide (PCOOH) was studied intensively to delineate its role in the altered pathophysiology of liver failure associated with endotoxemic shock. Endotoxemia was induced by cecal ligation and puncture (CLP) in three models using rats. Model 1 consisted of normal healthy rats; model 2, cirrhotic rats; and model 3, rats treated with catalase and superoxide dismutase (SOD). Samples were taken before CLP, then 12 h and 24 h following CLP. A progressive and significant increase in serum endotoxin was seen in all models; however, a significantly low energy charge (EC) and high PCOOH were seen in models 1 and 2, whereas no change was observed in model 3. The regional blood flow remained unchanged throughout the experiment in models 1 and 3, but not in model 2. An initial increase in alpha-tocopherol was seen in model 1. The survival rate was markedly better in model 3 than in models 1 or 2. The fall in EC corresponded to the increase in serum endotoxin as well as to the increase in tissue PCOOH in models 1 and 2. It was more likely that the elevated lipid peroxidation in model 1 resulted from endotoxemia rather than from tissue hypoperfusion. The early increase in alpha-tocopherol that occurred in models 1 and 2, but not in model 3, indicated the antiradical defense response to oxidative injury. Thus, antioxidant therapy significantly improved the survival rate and tissue adenine nucleotide level in spite of the increased serum endotoxin level.

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The Incidence of Decreased Red Blood Cell Deformability in Sepsis and the Association With Oxygen Free Radical Damage and Multiple-System Organ Failure

Cited by 108 publications

References 14 publications

Plasma Catalytic Iron, AKI, and Death among Critically Ill Patients

Plasma Catalytic Iron, AKI, and Death among Critically Ill Patients

Oxidative Stress Induced by Organo Sliver Clay Particles in Mice

Hepatic phosphatidylcholine hydroperoxide content in noncirrhotic, cirrhotic, and antioxidant-treated rats with endotoxemia

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