2002
DOI: 10.1055/s-2002-32404
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Elastase Release Following Myocardial Ischemia during Extracorporeal Circulation (ECC) - Marker of Ongoing Systemic Inflammation?

Abstract: Our results indicate that CPB initiates an elastase release that can be suppressed by prostacyclin. Increased intraoperative elastase levels in patients with PPS show that elastase may be an indicator of ongoing systemic inflammation, possibly causing complications due to a hypercoagulatory state. Myocardial ischemia seems to be one reason for this elastase release. It can be speculated that early PGl2-infusion could be a therapeutic option in inflammatory diseases caused by ECC.

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Cited by 9 publications
(2 citation statements)
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“…During extracorporeal circulation with CPB a marked increase in the level of polymorphonuclear (PMN) granulocytes elastase was reported as a result of cell activation and the release of elastase from azurophilic granules [26]. In resting neutrophils, uPAR molecules are stored in secretory vesicles and specific azurophilic granules, similarly with elastase, and rapidly translocate upon neutrophil activation to the cell surface [27].…”
Section: Discussionmentioning
confidence: 99%
“…During extracorporeal circulation with CPB a marked increase in the level of polymorphonuclear (PMN) granulocytes elastase was reported as a result of cell activation and the release of elastase from azurophilic granules [26]. In resting neutrophils, uPAR molecules are stored in secretory vesicles and specific azurophilic granules, similarly with elastase, and rapidly translocate upon neutrophil activation to the cell surface [27].…”
Section: Discussionmentioning
confidence: 99%
“…Although we measured neither endotoxin nor any inflammatory markers, it is conceivable that a systemic inflammatory response syndrome or endotoxemia provoked by the extracorporeal circulation may have contributed to the impaired hepatic oxygen extraction (22,24,29,30).…”
Section: Discussionmentioning
confidence: 99%