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Nikolaos G Baikoussis1, Nikolaos A Papakonstantinou2, Chrysoula Verra3, Georgios Kakouris3, Maria Chounti4, Panagiotis Hountis5, Panagiotis Dedeilias1, Michalis Argiriou1
1 Department of Cardiovascular and Thoracic Surgery, "Evangelismos'' General Hospital of Athens, Athens, Greece
2 Department of General Surgery, Agioi Anargiroi General Hospital, Kifissia, Athens, Greece
3 Department of Medical Biopathology, Patras General Hospital, Patras, Greece
4 Nursing School Technological Institute of Patras, Patras, Greece
5 Department of Thoracic and Cardiovascular Surgery, Athens Naval and Veterans Hospital, Athens, Greece
Correspondence Address:
Nikolaos G Baikoussis
45 47, Ipsilantou Street, Kolonaki, Athens
Greece
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0971-9784.166465
Cold heart protection via cardioplegia administration, limits the amount of oxygen demand. Systemic normothermia with warm cardioplegia was introduced due to the abundance of detrimental effects of hypothermia. A temperature of 32-33°C in combination with tepid blood cardioplegia of the same temperature appears to be protective enough for both; heart and brain. Reduction of nitric oxide (NO) concentration is in part responsible for myocardial injury after the cardioplegic cardiac arrest. Restoration of NO balance with exogenous NO supplementation has been shown useful to prevent inflammation and apoptosis. In this article, we discuss the "deleterious" effects of the oxidative stress of the extracorporeal circulation and the up-to-date theories of "ideal'' myocardial protection.
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