Cardioplegia does not prevent reperfusion injury induced by intracoronary platelet deposition.
We have shown that after global myocardial ischemia, reperfusion injury may be related to platelet deposition in the coronary microcirculation. The purpose of this study was to determine whether multidose hypothermic potassium cardioplegia suppresses platelet deposition during postischemic reperfusion. Platelets labeled with 111In and erythrocytes labeled with 51Cr were injected into dogs subjected to either 120 min of continuous cardiopulmonary bypass (control, n = 4), 60 min of global normothermic myocardial ischemia followed by 50 min of reperfusion (n = 6), or global ischemia with cardioplegia (n = 5). Intracoronary platelet deposition was determined by comparing the double-labeled isotope activity of myocardial biopsy specimens to peripheral blood. Reperfusion after global myocardial ischemia resulted in substantial deposition of platelets within the coronary vasculature in both the cardioplegia-treated (215 +/- 40 platelets/mg) and untreated (269 +/- 95 platelets/mg) groups. These increases were significantly greater than those measured during continuous bypass (48 +/- 2 platelets/mg; p less than .01). Cardioplegia, despite apparent washout of the microcirculation, does not alter platelet deposition. Thus other platelet-stabilizing measures must be used to prevent platelet deposition-induced reperfusion injury after surgical global ischemia.
D000818:Animals; D001792:Blood Platelets / Q000473:pathology*; D002315:Cardiopulmonary Bypass; D002860:Chromium Radioisotopes; D003326:Coronary Circulation; D004176:Dipyridamole / Q000627:therapeutic use*; D004285:Dogs; D004912:Erythrocytes / Q000473:pathology; D006324:Heart Arrest, Induced / Q000009:adverse effects*; D007204:Indium; D009206:Myocardium / Q000473:pathology; D010477:Perfusion / Q000009:adverse effects; D010976:Platelet Count; D011868:Radioisotopes
D002860:Chromium Radioisotopes; D011868:Radioisotopes; D007204:Indium; D004176:Dipyridamole