Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Keh,; Gerlach,; Kürer,; Spielmann,; Kerner,; Busch, David R.; Hansen, Richard A.; Falke,

doi:10.1046/j.1365-2362.1999.00459.x

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…Others have also suggested that platelet activation and the expression of platelet Pselectin are important steps in the formation of PLAs (41,42). Indeed, the present findings support previous studies that inhaled NO can decrease both platelet Pselectin expression and fibrinogen binding to the platelet glycoprotein IIb/IIIa receptor in healthy volunteers and critically ill patients (4,25,43,44). The significant correlation between the inhibition of PLA formation and the inhibition of P-selectin expression found in the present study provides more evidence that inhibition of P-selectin expression mediates inhibition of PLA formation in critically ill patients.…”

Section: Discussionsupporting

confidence: 92%

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Gries

Herr

Kirsch

et al. 2003

Critical Care Medicine

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Section: Discussionsupporting

confidence: 92%

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Gries

Herr

Kirsch

et al. 2003

Critical Care Medicine

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“…There are many different strategies to locally provide NO for precise PLT inhibition. A simple approach is the delivery of NO via sweep gas [22,23]. The direct generation of NO can also be achieved by surface modification, whereas the NO-donor species (e.g., diazeniumdiolates) are impregnated, blended or covalently incorporated in polymeric scaffolding blood-contacting materials [20,24].…”

Section: Introductionmentioning

confidence: 99%

Endogenous Nitric Oxide-Releasing Microgel Coating Prevents Clot Formation on Oxygenator Fibers Exposed to In Vitro Blood Flow

et al. 2022

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Background: Clot formation on foreign surfaces of extracorporeal membrane oxygenation systems is a frequent event. Herein, we show an approach that mimics the enzymatic process of endogenous nitric oxide (NO) release on the oxygenator membrane via a biomimetic, non-fouling microgel coating to spatiotemporally inhibit the platelet (PLT) activation and improve antithrombotic properties. This study aims to evaluate the potential of this biomimetic coating towards NO-mediated PLT inhibition and thereby the reduction of clot formation under flow conditions. Methods: Microgel-coated (NOrel) or bare (Control) poly(4-methyl pentene) (PMP) fibers were inserted into a test channel and exposed to a short-term continuous flow of human blood. The analysis included high-resolution PLT count, pooled PLT activation via β-Thromboglobulin (β-TG) and the visualization of remnants and clots on the fibers using scanning electron microscopy (SEM). Results: In the Control group, PLT count was significantly decreased, and β-TG concentration was significantly elevated in comparison to the NOrel group. Macroscopic and microscopic visualization showed dense layers of stable clots on the bare PMP fibers, in contrast to minimal deposition of fibrin networks on the coated fibers. Conclusion: Endogenously NO-releasing microgel coating inhibits the PLT activation and reduces the clot formation on PMP fibers under dynamic flow.

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“…Other investigators have since corroborated this finding by performing similar in vitro experiments. 15 This phenomenon demonstrates the non-thrombogenic effect of NO administered through an active membrane, but as of present this has not been applied clinically because the rest of the ECLS circuitry remains thrombogenic.…”

Section: Mimicking the Endothelium-the Use Of Nitric Oxide (No) To Prmentioning

confidence: 96%

The artificial endothelium

Reynolds

Annich

2011

Organogenesis

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As the world of critical care medicine advances, extracorporeal therapies (ECC) have become commonplace in the management of the high risk intensive care patient. ECC encompasses a wide variety of technologies from hemodialysis, continuous renal replacement therapy (CRRT) and plasmapheresis, to cardiopulmonary bypass (CPB), extracorporeal life support (ECLS) and hepatic support. The development of internal man made organs is the next step with ventricular assist devices and artificial lungs. As we advance the technologies with smaller devices, and more intricate circuitry, we lack the keystone necessary to control the blood-biomaterial interface. For the last 50 years much has been learned about surface induced thrombosis and attempts have been made to prevent it with alternative systemic anticoagulation, circuitry surface modifications, or a combination of both. Despite these efforts, systemic or regional anticoagulation remain necessary for both laboratory and clinical application of ECC. As such, the development of an endothelial-like, biomimetic surface to reduce or perhaps even eliminate the blood activation/thrombus formation events that occur upon exposure to artificial surfaces is paramount.

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Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation

Abstract: Transmembranous diffusion of gaseous NO revealed protective effects on platelets by reducing thrombocytopenia/pathia and preserving platelet reactivity.

Cited by 13 publications

References 32 publications

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome

Endogenous Nitric Oxide-Releasing Microgel Coating Prevents Clot Formation on Oxygenator Fibers Exposed to In Vitro Blood Flow

The artificial endothelium

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