Evaluation of the Biocompatibility of a New Method for Heparin Coating of a Cardiopulmonary Bypass Circuit

Takano, Hiroshi; Nakano, Susumu; Kadoba, Keishi; Kaneko, Mai; Miyamoto, Yusuke; Ohtake, Shigeaki; Matsuwaka, R; Jc, Chang; Amemiya, Akira; Matsuda, Hiroyuki

doi:10.1097/00002480-199207000-00062

Cited by 9 publications

(6 citation statements)

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“…The heparin-coated group circuit consisted of polyvinyl chloride tubing connected to the soft-shell venous reservoir and the oxygenator Capiox SX18H (Terumo). The entire blood-contacting surface was covalently bonded with heparin (12). The uncoated group circuit consisted of polyvinyl chloride tubing connected to the soft-shell venous reservoir and the oxygenator Capiox SX18 (Terumo).…”

Section: Groupsmentioning

confidence: 99%

Effects of New Polymer‐Coated Extracorporeal Circuits on Biocompatibility During Cardiopulmonary Bypass

2000

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An inflammatory response due to bioincompatibility of extracorporeal circuits is a major clinical issue during cardiopulmonary bypass (CPB). By using a swine model, we determined whether new polymer-coated circuits, the blood-contacting surfaces of which are coated with poly(2-methoxyethylacrylate) (PMEA), would reduce the inflammatory response during CPB. Plasma bradykinin levels and the percentages of CD35-positive monocytes in PMEA-coated circuits were significantly lower than those in uncoated circuits during CPB. The amount of proteins adsorbed on the PMEA-coated circuits was significantly lower than that on the uncoated circuits (0.30 microg/cm2 versus 3.42 microg/ cm2). Almost no IgG, IgM, or C3c/d was detected in proteins adsorbed on the PMEA-coated circuits although these proteins were clearly detected in proteins adsorbed on the uncoated circuits. We concluded that PMEA coating could reduce complement activation during CPB by suppressing the adsorption of IgG and IgM, which activate C3 via the classical pathway, on the surface of the circuits.

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Section: Groupsmentioning

confidence: 99%

Effects of New Polymer‐Coated Extracorporeal Circuits on Biocompatibility During Cardiopulmonary Bypass

2000

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“…15 Hence, factors other than blood-material contact must be involved. By monitoring platelet aggregation continuously, we were recently able to demonstrate that platelets in human and rat blood are activated by use of a roller pump.…”

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confidence: 99%

Hypotension Caused by Extracorporeal Circulation

2002

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Background-Cardiopulmonary bypass and hemodialysis often cause hypotension. We investigated a possible role of pump-induced platelet activation with consequent serotonin release. Methods and Results-In rats, a heparin-coated extracorporeal shunt was placed between the proximal part of a carotid artery and the distal part of a femoral artery. Autoperfusion did not affect platelets or hemodynamics. Pump perfusion, however, immediately elicited strong platelet aggregation, whereas aortic pressure rapidly fell to 60Ϯ12% (meanϮSD) of its prepump value, partially recovered, and then progressively decreased to 70Ϯ12% at 2 hours. Femoral resistance doubled and then decreased to 59Ϯ11%. The initial changes in aortic pressure and femoral resistance were proportional to the amount of platelet aggregation, were accompanied by a rise (6-fold) in plasma serotonin levels downstream of the pump, but not in the aorta, and could be mimicked by serotonin-infusion into the leg. All hemodynamic changes were prevented or largely reduced by blockade of 5-hydroxytryptamine (5-HT) 2 receptors with pizotifen or ritanserin. The hypotension and femoral resistance decrease could also be prevented or abolished by inhibiting the production of nitric oxide (NO), an intermediate in 5-HT 2B receptor-induced vasodilation. When the extracorporeal blood was pumped into the aortic arch instead of the femoral artery, the hypotensive effect was similar and also NO dependent, but it was absent with venous return. Conclusions-Pump perfusion with arterial return of the blood causes hypotension by endothelial NO-release, which in turn is triggered by serotonin from activated platelets.

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“…Bleeding disorders have been attributed to thrombocytopenia and platelet dysfunction caused by platelet adhesion 1,2 and contact activation. [3][4][5] Coating the system with heparin reduces complement activation, [6][7][8] platelet adhesion, [9][10][11] and Objective: Coating of extracorporeal systems with heparin does not prevent platelet activation and subsequent bleeding disorders. We investigated whether this could be due to elevated shear stress caused by a roller pump.…”

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confidence: 99%

“…Albumin coating has been reported to be as effective as heparin coating in preventing platelet aggregation and activation as a result of blood-material contact. 2,9,10,23 To elucidate the role of shear stress we studied whether pump-induced platelet aggregation could be prevented with aurintricarboxylic acid (ATA), a synthetic triphenylmethane dye that specifically prevents shear-induced platelet aggregation without affecting aggregation induced by ADP, collagen, epinephrine, thrombin, or arachidonic acid. 24,25 Experiments were done with human blood in vitro and with rat blood in vitro and in vivo.…”

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confidence: 99%