الفهرس Only 14 pages are availabe for public view
 |  | from | 213 |  |  |
| | | from | 213 | | |
Abstract
SUMMARY
Cardiac surgery and cardio pulmonary bypass (CPB) activate a systemic inflammatory response characterized clinically by alterations in cardiovascular and pulmonary function.
Most patients undergoing CPB experience some degree of organ dysfunctions as a result of activation of the inflammatory response.
The systemic inflammatory response may be initiated during cardiac surgery by a number of processes including blood contact with the foreign surface of the CPB apparatus, development of isocheimal and reperfusion injury and the presence of end toxemia, which contribute to the humoral and cellular development of the process, the extent and duration of the response is influenced by many factor including pharmacological agents used to ameliorate the response e.g. glucocorticoids (methylprednisolone, dexamethazone), protease inhibitors (apportioning), gut therapy (selective gut decontamination with polymyxin E, tobramycine, amphotericin B, or laxatives), pentoxifylline, immunomodulation (indomethacin thiopental), antioxidants and mechanical strategies i.e. the presence of pulsate perfusion, the use of mechanical filtration (with filtration, leukocyte depleting filters), the type of oxygenate (membrane or bubble), the type of extra corporeal circuit (Heparin bonded-silicone coated), the temperature during CPB (warm, moderate, mild hypothermia) and the composition of the CPB priming solution (crystalloids, fresh frozen plasma, colloids). CPB has been shown to induce complement activation, emoting release, leukocyte activation, the expression of adhesion molecules and the release of many inflammatory mediators including oxygen free-radicals, arachidonic acid metabolites, platelet activating factor, nitric oxide, endothelins and cytokines.
The systemic inflammatory response after cardiopulmonary bypass can be characterized by the production of pro-inflammatory and anti- inflammatory cytokines.