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Effect Of Brain Death On S-nitrosohemoglobin And Tissue Perfusion: A Prospective Study For Evaluation Of A Novel Therapeutic Target To Increase VCA Availability
Mohamed Awad, MD, Ryan Nazemian, MD, Edwin Colon, James Reynolds, PhD, Anand Kumar, MD.
Case Western Reserve University, Cleveland, OH, USA.

Background: Brain Dead (BD) results in physiological instability due to intense sympathetic stimulation and significant release of catecholamines (Cushing Response) we have postulated that BD induces a significant disruption of systemic S-nitrosothiol (SNO) homeostasis which regulates local blood flow. Our lab has demonstrated that decreased levels and/or impaired processing of S-Nitrosohemoglobin (SNO-Hb) have been observed in diseases characterized by tissue hypoxemia and after brain death. We hypothesized that brain death donors have a significant decrease in SNO levels compared to healthy controls.
Methods: In prospective cohort study, we recruited two groups: healthy adult volunteer (n=9) vs adult DNC donors (n=63) provided to the research team by Lifebanc, the North East Ohio Organ Procurement Organization. Serial measurements of S-nitroso-hemoglobin (SNO-Hb) were collected during donor support phase. SNO-Hb levels measured by mercury-coupled photolysis-chemiluminescence technique, data analyzed using R software.
Results: SNO-Hb levels in DNC donors (mean 2.4g/dl) is significantly (p < 0.05) lower than SNO-Hb levels in healthy individuals (mean 4.2 g/dl). Total NO (XNO) and NO bound to Heme Iron (FeNO), were also significantly lower in brain death donors compared with healthy individuals.
Conclusion: Brain-death significantly disturb SNO-Hb level. This highlights the possibility that repletion of SNO-Hb by S-nitrosylating agent may help to maintain tissue oxygenation, reduce tissue injury and organ damage in brain dead donors which may subsequently, increase the number of organs/tissue recovered for transplant.


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