PubMed · 8642725
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J M Lusher, S Sarnaik. 1996-06-19. Hematology.. https://pubmed.ncbi.nlm.nih.gov/8642725/
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PURPOSE: Modified ultrafiltration (MUF) after cardiopulmonary bypass (CPB) in children has been reported to reduce the need for postoperative blood transfusion and minimize postoperative blood loss. This study was undertaken to quantify the effects of MUF on coagulation factors in pediatric patients. METHODS: Seven children scheduled to undergo open-heart surgery for congenital heart defects were studied. CPB circuits were primed with crystalloid solutions and no blood transfusions were performed. Hematocrit, platelet count, total plasma proteins, albumin, fibrinogen, prothrombin, factor VII, factor IX, and factor X were measured preoperatively, at the termination of cardiopulmonary bypass, and at the end of modified ultrafiltration. RESULTS: MUF was associated with significant (P < 0.05) increases in hematocrit (17.6% +/- 1.6% to 21.6% +/- 2.4%), platelet count 11.1 +/- 2.5 to 12.8 +/- 2.4 x 10(4)/mm3), total plasma proteins (2.7 +/- 0.3 to 3.4 +/- 0.4 g/dl), and albumin (1.6 +/- 0.2 to 2.1 +/- 0.2 g/dl). Fibrinogen, prothrombin, and factor VII also increased significantly (P < 0.05) during MUF, but factor IX and factor X did not change. CONCLUSION: We conclude that MUF attenuates the dilutional coagulopathy that occurs during CPB in children. There were slight improvements in the coagulation factors when MUF was employed.
Circulating monocytes as well as resident monocyte-derived macrophages (MDMs) in the atherosclerotic plaque express tissue factor. We tested the hypothesis that differentiation of monocytes into macrophages increases their tissue factor expression. This was done by isolating monocytes from human blood and culturing them for 24 h or allowing their differentiation into macrophages for 8 days before assay. Tissue factor procoagulant activity was assessed by recalcification clotting assay while Western blotting quantitated tissue factor protein. Immunocytochemistry was applied to localize antigenic tissue factor in cells. The results showed that freshly-isolated monocytes expressed low baseline procoagulant activity (0.0004+/-0.0003 ng rhTF/10(6) cells) which increased 100-fold in 24-h cultured monocytes (0.04+/-0.01 ng/10(6) cells, P<0.0001) and was associated with detectable tissue factor protein by Western blotting. Furthermore, MDMs expressed 25-fold higher procoagulant activity (1.0+/-0.5 ng/10(6) cells, P<0.04) and increased tissue factor protein content compared with 24-h monocytes as corroborated by immunocytochemistry. LPS stimulation increased baseline binding activity of transcription factor kappaB three-fold (P<0.03) and 2.6-fold (P<0.09) in monocytes and in macrophages, respectively. The results demonstrate that differentiation of human monocytes into macrophages in culture enhances their tissue factor expression. The observed tissue factor increase that can be further stimulated by LPS may contribute to thrombogenicity of macrophage-rich atheroma. Activation of the TF-kappaB transduction pathway suggests its potential role in the transcriptional regulation of TF gene in response to acute stimulation in these cells. This cell-culture model may provide the opportunity to evaluate the effect of various interventions on macrophage procoagulant activity.