CHANGES IN PERICARDIAL MORPHOLOGY AND FIBRINOLYTIC-ACTIVITY DURING CARDIOPULMONARY BYPASS

The presence of pericardial adhesions at resternotomy not only increas es the operation time but also increases the risk of serious damage to the heart, great vessels, and extracardiac grafts. The reported preva lence of damage is 2% to 6%. The fibrinolytic activity of pericardial tissue may be a crucial factor in determining the extent of adhesion f ormation following primary operation. Ten patients undergoing cardiac operations were studied to assess the plasminogen activating activity of homogenates of pericardial tissue samples. Samples were taken at th ree times during the operation and the plasminogen activating activity was measured by means of a standard fibrin plate technique. Tissue-ty pe plasminogen activator, urokinase-type plasminogen activator, plasmi nogen activator inhibitor-1, and plasminogen activator inhibitor-2 wer e also measured by means of enzyme-linked immunosorbent assays. Compar ed with its initial levels (median 2.06 IU/cm2 range 1.28 to 6.48 IU/c m2), the plasminogen activating activity of pericardial biopsy tissue was significantly reduced at 75 minutes (median 0.64 IU/cm2, range 0.1 2 to 2.44 IU/cm2, p < 0.01) and at 135 minutes (median 1.45 IU/cm2, ra nge 0.12 to 4.39 IU/cm2, p < 0.05). The major plasminogen activator pr esent was tissue-type plasminogen activator. Compared with its initial levels (median 2.34 ng/ml, range 1.03 to 6.42 ng/ml), subsequent tiss ue-type plasminogen activator values were also significantly reduced a t 75 minutes (median 0.83 ng/ml, range 0.75 to 5.13 ng/ml, p < 0.005) and at 135 minutes (median 1.24 ng/ml, range 0.75 to 6.67 ng/ml, p < 0 .05). Low levels of urokinase-type plasminogen activator were found in 5 of 10 patients. However, neither plasminogen activator inhibitor-1 nor plasminogen activator inhibitor-2 was detected. Examination with a light microscope showed both increasing pericardial mesothelial damag e and increasing features of acute inflammatory changes with time. Thi s study shows that plasminogen activating activity is present in peric ardial tissue and that tissue-type plasminogen activator is the major plasminogen activator. The observed inflammatory changes and concomita nt damage to the pericardial mesothelium, and the significant reductio ns in pericardial tissue-type plasminogen activator and plasminogen ac tivating activity seen during cardiac operations, may be important fac tors contributing to the early development of pericardial adhesions.