James K Kirklin, MD, David C McGiffin, MD

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Control of the inflammatory response in extended myocardial preservation of the donor heart James K Kirklin, MD, David C McGiffin, MD The Annals of Thoracic Surgery Volume 68, Issue 5, Pages 1978-1982 (November 1999) DOI: 10.1016/S0003-4975(99)01016-4

Fig 1 Proposed mechanisms of donor cardiac ischemic and reperfusion injury. The Annals of Thoracic Surgery 1999 68, 1978-1982DOI: (10.1016/S0003-4975(99)01016-4)

Fig 2 Plasma levels of C3a in patients undergoing cardiopulmonary bypass. (Reprinted with permission from Chenoweth DE, Cooper SW, Hugli TE, Stewart RW, Blackstone EH, Kirklin JW. Complement activation during cardiopulmonary bypass. N Engl J Med 1981;304:497–503.) The Annals of Thoracic Surgery 1999 68, 1978-1982DOI: (10.1016/S0003-4975(99)01016-4)

Fig 3 Model of the sequential steps in adhesion of neutrophils to the endothelium and the underlying molecular mechanisms. (Reprinted from Hansen PR. Role of neutrophils in myocardial ischemia and reperfusion. Circulation 1995;91:1872–85 with permission.) The Annals of Thoracic Surgery 1999 68, 1978-1982DOI: (10.1016/S0003-4975(99)01016-4)

Fig 4 Endothelial cells produce and secrete several factors under normal circumstances to maintain the vessel integrity. During ischemia or injury, there is a decrease in the production of nitric oxide and prostacyclin but an increase in the production of endothelin. There is also an activation of leukocytes and an increase in the presence of endothelial adhesion molecules. In reperfusion injury, there is leukocyte adherence, movement through vascular intima, capillary leakage, and production of cytokines, prostanoids, and superoxides that cause further cellular damage, edema, and fluid sequestration. (Reprinted with permission from McMillen MA, Huribal M, Sumpio B. Common pathway of endothelial-leukocyte interaction in shock, ischemia, and reperfusion. Am J Surg 1993;166:557–62.) The Annals of Thoracic Surgery 1999 68, 1978-1982DOI: (10.1016/S0003-4975(99)01016-4)

Fig 5 Schematic representation of important inflammatory mediators with cardiotoxic potential released from activated neutrophils. O2− = superoxide anion; HOCl = hypochlorous acid; H2O2= hydrogen peroxide; MPO =myeloperoxidase; E = elastase; C = collagenase; LTB4 = leukotriene B4; PAF = platelet-activating factor. (Reprinted from Hansen PR. Role of neutrophils in myocardial ischemia and reperfusion. Circulation 1995;91:1872–85 with permission.) The Annals of Thoracic Surgery 1999 68, 1978-1982DOI: (10.1016/S0003-4975(99)01016-4)