In Vitro Inhibition of Platelet Aggregatton by the Gelatin Plasma Expander Haemaccel.(R)

1979 ◽  
Author(s):  
I. Stibbie ◽  
P.M. van der Plas ◽  
G.L. Ong ◽  
D.S. de Jong ◽  
E. Krenning-Douma ◽  
...  

In a study concerning open-heart surgery we found that, platelet aggregates present in heparinised human blood disappeared immediately after addition of the gelatin plasma expander haemaccel. A study was therefore initiated of the effect of haemaccei on platelet appregation (Payton apprepometer, 4W RPM as controlled by stroboscope, 37°C, final platelet count 200-300 χ 109/1) and compared with the effect of bovine serum albumin (USA) and platelet poor plasma (PPP). Haemaccel powder was kindly supplied by Rehringwerke and contained 0.98% sodium, 0.015% calcium and no measurable potassium. 0.3 ml human platelet rich plasma (PRP) was nixed with 0.2 ml haemaccel (final concentrations 0-20 mg/ml) in Tyrode’s solution (2 mM Ca++. pH 7,4), Haemaccel inhibited apgrepation in both citrated and heparinised PRP induced by collagen, ADP or adrenalin, both in the presence or absence of indomethacin (90/μM), PPP (0.2 ml) and BSA (in Tyrode’s solution, final concentrations 0-16 mp/ml) were also inhihitinp, hut on a weipht hasis less than haemaccel. Different Ca++ concentrations in the Tyrode’s solution did not alter the inhibition by haemaccel. Final pH in aggregation mixtures varied by less than 0.10 for a given experiment. It is concluded that, under the conditions used, haemaccel and USA inhibit platelet appregation, probably by a non-specific mechanism.

2019 ◽  
Vol 8 (7) ◽  
pp. 1028 ◽  
Author(s):  
Tak-Wah Wong ◽  
Chung-Dann Kan ◽  
Wen-Tai Chiu ◽  
Kin Lam Fok ◽  
Ye Chun Ruan ◽  
...  

Human cardiac progenitor cells isolated from the same host may have advantages over other sources of stem cells. The aim of this study is to establish a new source of human progenitor cells collected from a waste product, pericardiac effusion fluid, after open-heart surgery in children with congenital heart diseases. The fluid was collected every 24 h for 2 days after surgery in 37 children. Mononuclear cells were isolated and expanded in vitro. These pericardial effusion-derived progenitor cells (PEPCs) exhibiting cardiogenic lineage markers, were highly proliferative and enhanced angiogenesis in vitro. Three weeks after stem cell transplantation into the ischemic heart in mice, cardiac ejection fraction was improved significantly without detectable progenitor cells. Gene expression profiles of the repaired hearts revealed activation of several known repair mechanisms including paracrine effects, cell migration, and angiogenesis. These progenitor cells may have the potential for heart regeneration.


2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Alison L Müller ◽  
Darren H Freed

There are many cell types that can contribute to cardiac fibrosis including atrial fibroblasts (AFs) and bone marrow-derived progenitor cells (MPCs). We have previously shown that MPCs display a myofibroblast phenotype in vitro which is linked to altered microRNA(miR)-301a expression, a miR affiliated with maintaining proliferation in numerous cell types. We have also shown that miR-301a influences a dichotomous phenotype in primary human MPCs isolated from patients undergoing open heart surgery. As both MPCs and AFs display a dichotomous phenotype where each cell type displays a phenotype that pathologically contributes to fibrosis, we transfected both MPCs and AFs with miR-301a. AFs were also isolated from patients undergoing open heart surgery. We observed decreases in levels of both mRNA and protein of collagen I, non-muscle myosin IIA, and EDA-fibronectin. These proteins are expressed in myofibroblasts, the cell type predominantly responsible for causing cardiac fibrosis. In addition, transfection of miR301a caused both cell types to increase proliferation, which was analyzed using MTT proliferation assays. These results indicate that miR-301a could be influencing a non-fibrotic phenotype, which could prove useful in cell therapy trials where progenitor cells are injected into scar tissue in order to help heal patients who have suffered from a myocardial infarction. Over-expressing miR-301a in cells used could prevent them from differentiating into pro-fibrotic phenotypes and encourage their proliferation, thereby potentiating their efficacy.


2000 ◽  
Vol 24 (3) ◽  
pp. 182-184 ◽  
Author(s):  
Waldyr Parolari Novello ◽  
Maria Helena Santana ◽  
Antonio Celso Fonseca de Arruda

1978 ◽  
Vol 39 (02) ◽  
pp. 474-487 ◽  
Author(s):  
E R Cole ◽  
F Bachmann ◽  
C A Curry ◽  
D Roby

SummaryA prospective study in 13 patients undergoing open-heart surgery with extracorporeal circulation revealed a marked decrease of the mean one-stage prothrombin time activity from 88% to 54% (p <0.005) but lesser decreases of factors I, II, V, VII and X. This apparent discrepancy was due to the appearance of an inhibitor of the extrinsic coagulation system, termed PEC (Protein after Extracorporeal Circulation). The mean plasma PEC level rose from 0.05 U/ml pre-surgery to 0.65 U/ml post-surgery (p <0.0005), and was accompanied by the appearance of additional proteins as evidenced by disc polyacrylamide gel electrophoresis of plasma fractions (p <0.0005). The observed increases of PEC, appearance of abnormal protein bands and concomitant increases of LDH and SGOT suggest that the release of an inhibitor of the coagulation system (similar or identical to PIVKA) may be due to hypoxic liver damage during extracorporeal circulation.


1967 ◽  
Vol 18 (03/04) ◽  
pp. 634-646 ◽  
Author(s):  
N Thurnherr

SummaryBlood clotting investigations have been executed in 25 patients who have undergone open heart surgery with extracorporeal circulation. A description of alterations in the activity of blood clotting factors, the fibrinolytic system, prothrombin consumption and platelets during several phases of the operation is given.


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