الفهرس 
A NATOMY OF C ORONARY A RTERIESOnly 14 pages are availabe for public view
 |  | from | 113 |  |  |
| | | from | 113 | | |
Abstract
Myocardial ischemia-reperfusion injury (IRI) will always be one of the big challenges that we face during cardiopulmonary bypass (CPB) and cardioplegic arrest (CA). It affects both cardiac myocytes and coronary endothelial cells and is considered to be a major factor contributing to perioperative myocardial damage. The massive release of oxygen free radicals during the early phase of reperfusion is the source of these injuries.
The term myocardial protection refers to strategies and methodologies used either to attenuate or to prevent post ischemic myocardial dysfunction that occurs during and after major aortic surgeries that need CPB.
Ischemic preconditioning is an adaptive biologic phenomenon in which the heart (and numerous other tissues) becomes more tolerant to a period of prolonged ischemia if first exposed to a prior episode of brief ischemia and reperfusion. This adaptation to ischemia was described as classic or early-phase preconditioning. This increased tolerance to ischemia is associated with a reduction in infarct size, apoptosis, and reperfusion-associated arrhythmias. It appears to persist as long as 1 to 2 hours after the ischemic preconditioning stimulus. It becomes ineffective when the sustained ischemic insult exceeds 3 hours.
An additional observation that ischemia induced in other organs could precondition the heart, a phenomenon referred to as remote or interorgan preconditioning. Remote myocardial preconditioning can be induced by brief occlusions of the renal and mesenteric arteries, as well as by skeletal muscle ischemia.
Remote ischemic preconditioning (RIPC) represents a strategy for harnessing the body’s endogenous protective capabilities against the injury incurred by ischemia and reperfusion. It describes the intriguing phenomenon in which transient non-lethal ischemia and reperfusion of one organ or tissue confers resistance to a subsequent episode of lethal ischemia reperfusion injury in a remote organ or tissue.
Several agents have been used to protect the myocardium and minimize the damage during CPB. Dexmedetomidine and sevoflurane were among these agents. Several reports have suggested that their use could manage clinical conditions as IRI and inflammation related complications after CPB. Also, their perioperative administration could decrease infarct size following a prolonged ischemic insult and improve post-ischemic functional recovery (i.e. myocardial stunning) associated with decreased postoperative mortality and shorter length of hospital stay after major aortic surgeries that need CPB.