Abstract
An abnormal elevation in pressure is a serious complication involving the extracorporeal circulation circuit. Clot formation might be associated with this complication, but the precise mechanism of an abnormal elevation in pressure has not been identified. We investigated sufficient conditions for in-circuit elevation in pressure using an ex vivo re-circulation circuit with porcine blood. Specifically, we investigated the effect of blood conditions, the type of anticoagulation, and pro-inflammatory stimulation on in-circuit pressure. We also examined the cause of an abnormal elevation of in-circuit pressure by specifically degrading DNA, RNA, or protein components of an obstructed filter and by using immunofluorescent techniques. Neither a change in temperature nor change in pH in the blood increased in-circuit pressure. In contrast, long-term storage of blood, pro-inflammatory stimulation by phorbol myristate acetate, and heparin administration significantly increased in-circuit pressure. Abnormal in-circuit elevation in pressure was associated with deposition of extracellular DNA on the outlet surface of the filter. Administration of DNase resulted in a rapid decline of in-circuit pressure. In an ex vivo re-circulation circuit system, extracellular DNA deposition on the filter is responsible for an abnormal in-circuit elevation in pressure. Senescent leukocytes, stimulated leukocytes, and heparin exposure are associated with extracellular DNA deposition.
Highlights
An abnormal elevation in pressure is a serious complication involving the extracorporeal circulation circuit
Long-term storage of blood significantly increased in-circuit pressure (p < 0.05) if blood was anticoagulated with heparin (Fig. 1B), while in-circuit pressure elevation was minimal if blood was anticoagulated with citrate (Fig. 1C)
These findings suggest that the storage term of blood and the type of anticoagulation may be associated with an abnormal elevation in pressure
Summary
An abnormal elevation in pressure is a serious complication involving the extracorporeal circulation circuit. Abnormal in-circuit elevation in pressure was associated with deposition of extracellular DNA on the outlet surface of the filter. In an ex vivo re-circulation circuit system, extracellular DNA deposition on the filter is responsible for an abnormal in-circuit elevation in pressure. To determine the underlying mechanisms of an abnormal elevation in pressure during CPB, we developed an extracorporeal recirculation circuit in which in-circuit pressure could be monitored and a filter could be removed and analyzed In this ex vivo circuit, we used a removable filter with a pore size of 40 μm because the pore sizes of a cardiotomy filter and arterial line filter in CPB equipment are approximately 40 μm, while the span of oxygenator fibers is approximately 50–250 μm. We found that extracellular DNA deposition on the outlet of the filter was responsible for the abnormal in-circuit elevation in pressure
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