The inflammatory response and extracorporeal circulation.
Defining the cause of organ and tissue dysfunction associated with the use of perfusion systems will produce methods of prevention or treatment and improve patient outcome. The problem is the plethora of triggers, effectors, and mediators in this process, which can now be measured. Each new measureable compound becomes another biochemical "smoking gun" without physiological data to show any relevance to the human problem. This review critically compares and contrasts the role of certain, largely novel, initiation, amplification, and cytotoxic mechanisms in the inflammatory response of the myocardium and pulmonary systems after a period of cardiopulmonary bypass. The available evidence strongly points to the process being different for each of these tissue beds. These data suggest that ensuring normal lung and heart functions after surgery will require separate therapeutic strategies.
Royston
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Department of Anaesthesia, Harefield Hospital, UK.
D001798:Blood Proteins / Q000502:physiology; D006348:Cardiac Surgical Procedures; D015815:Cell Adhesion Molecules / Q000502:physiology; D003167:Complement Activation; D016207:Cytokines / Q000502:physiology; D005112:Extracorporeal Circulation / Q000009:adverse effects*; D006321:Heart / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000517:prevention & control / Q000628:therapy; D007962:Leukocytes / Q000502:physiology; D008168:Lung / Q000502:physiology; D010586:Phagocytes / Q000502:physiology; D015427:Reperfusion Injury / Q000209:etiology; D019087:Selectins / Q000502:physiology; D016896:Treatment Outcome
D001798:Blood Proteins; D015815:Cell Adhesion Molecules; D016207:Cytokines; D019087:Selectins