Peer-Reviewed Publication
Mol Med2026;32(1)May 8, 2026Journal Article
Nitric oxide supplementation during extracorporeal resuscitation drives oxidative-inflammatory signaling and metabolic suppression in the post-cardiac arrest heart.
Abou Bakr M Salama1,2,3,4, Daniele Linardi5, Romel Mani5, Maddalena Tessari5, Qinghui Ou6, Yasmin Y Salem6, Ahmed Abdulsaboor7, Ahmed M Shaker8, Ahmad Gebreil6, Ahmed Elbakri9, Riham R E Abouleisa10, Bahaael El Sady11, Giovanni B Luciani5
1Cardiology Department, Faculty of Medicine, Zagazig University, Zagazig, Sharkia, Egypt. abobakr@aucegypt.edu.
2American University in Cairo, Cairo, Egypt. abobakr@aucegypt.edu.
3Cardiac Surgery Department, University of Verona, Verona, Italy. abobakr@aucegypt.edu.
4Surgery Department, Baylor College of Medicine, Houston, TX, USA. abobakr@aucegypt.edu.
5Cardiac Surgery Department, University of Verona, Verona, Italy.
6Institute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, KY, USA.
7Clinical Pathology Department, Faculty of Pharmacy, Zagazig University, Zagazig, Sharkia, Egypt.
8Physiology Department, National Research Institute, Cairo, Egypt.
9Valar Labs, Houston, TX, USA.
10Surgery Department, Baylor College of Medicine, Houston, TX, USA.
11Great Western Hospitals NHS Foundation Trust, Swindon, Wiltshire, UK.
Abstract
BACKGROUND: Myocardial dysfunction is a major determinant of mortality after cardiac arrest, yet the molecular events driving post-resuscitation injury remain incompletely understood. Nitric oxide (NO) has been proposed as a cardioprotective adjunct during extracorporeal life support (ECLS), but its mechanistic impact on myocardial recovery is unclear. We investigated whether NO supplementation du…
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