Chapter category: Heart
Harnessing the Cardioprotective Potential of Nitric Oxide in Nonsurgical and Surgical Ischemic-Reperfusion Injury
Ischemia-Reperfusion Injury in Cardiac Surgery
Edited by: Friedhelm BeyersdorfISBN: 1-58706-002-7
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Chapter authors:
Jakob Vinten-Johansen Russell S. Ronson
In cardiac surgery, there are numerous opportunities during the conduct of the operation for both unplanned and hence unprotected ischemia with subsequent reperfusion. These periods of potential injury include 1) antecedent ischemia (regional coronary occlusion, profound hypotension) occurring before institution of cardiopulmonary bypass or other means of hemodynamic support, 2) "protected" ischemia encountered between infusions of cardioplegia solution, but which may be complicated by maldistribution of cardioplegia solution by coronary obstructions or inadequate delivery pressures, and 3) inadvertent ischemia occurring after reperfusion has been initiated.1,2 Each ischemic event not only carries the potential for producing damage in its own right, but may also interact with each other in a cumulative fashion. Each interval of ischemia also carries the potential for subsequent reperfusion injury, defined as injury extending beyond that present during ischemia. Whether this is an active process of dynamic injury development leading to new necrosis or dysfunction, or whether reperfusion injury is simply a passive phenotypic expression of morphologic changes that have occurred during ischemia, and that interventions to alter reperfusion injury are altering the course of that expression are issues that are fervently debated.3,4 Therefore additional reperfusion injury may follow 1) resuscitation or hemodynamic restabilization before cardiopulmonary bypass, 2) infusion of cardioplegia solution through a newly revascularized segment, or initialization of blood flow through an internal mammary artery conduit, or 3) removal of the aortic cross clamp. The targets of ischemic-reperfusion injury are not restricted to myocytes alone in the form of necrosis or contractile dysfunction, but also include the vascular endothelium and its ability to elaborate important endogenous factors such as nitric oxide (NOï) and adenosine which are active in regulation of blood flow, blood pressure and cell-cell (neutrophil-endothelial cell) interactions.5 Additionally, extracorporeal circuits used in many cardiac surgical procedures contribute to the pathophysiology of ischemia and reperfusion injuries by activating complement and cytokines which recruit neutrophils and other inflammatory cells and thereby amplify the inflammatory process.6 This extracorporeal inflammatory component makes surgical ischemic-reperfusion injury uniquely different from its nonsurgical counterpart.
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Harnessing the Cardioprotective Potential of Nitric Oxide in Nonsurgical and Surgical Ischemic-Reperfusion Injury
Jakob Vinten-Johansen Russell S. Ronson
In cardiac surgery, there are numerous opportunities during the conduct of the operation for both unplanned and hence unprotected ischemia with subsequent reperfusion. These periods of potenti...
