Neutrophils and platelets accumulate in the heart, lungs, and kidneys after cardiopulmonary bypass in neonatal pigs

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OBJECTIVE: Cardiac surgery with cardiopulmonary bypass elicits a systemic inflammatory response. An exaggerated response is associated with organ dysfunction and increased morbidity and mortality.

DESIGN: The aim of the present study was to investigate whether the cardiopulmonary bypass procedure in itself results in accumulation of isotope-labeled platelets, polymorphonuclear neutrophils, and fibrinogen at organ levels in neonatal pigs and to monitor changes in organ function.

SETTING: Pediatric cardiopulmonary bypass setup with 60 mins of aortic cross-clamp time and 120 mins of hypothermic cardiopulmonary bypass time.

SUBJECTS: Thirty piglets were allocated to sternotomy alone (sham group, n = 15) or to sternotomy and cardiopulmonary bypass (n = 15).

MEASUREMENTS AND MAIN RESULTS: Isotope-labeled autologous polymorphonuclear neutrophils, platelets, and commercially available fibrinogen were infused, and the specific accumulation at organ level was measured in a gamma counter 4 hrs after termination of cardiopulmonary bypass. Concomitant changes in oxygenation index and cardiac output were registered. Animals exposed to cardiopulmonary bypass showed a significantly higher technetium-99m-polymorphonuclear neutrophil accumulation in the lungs and kidneys, whereas indium-111-platelets accumulated in the heart and kidneys compared with the sham group. There was a significantly larger increase in oxygenation index and significantly larger decrease in cardiac output between the pre- and postcardiopulmonary bypass period in the cardiopulmonary bypass group compared with the sham group.

CONCLUSIONS: The cardiopulmonary bypass procedure without cardiac surgery elicits organ dysfunction in terms of impaired respiratory and hemodynamic function. Platelets and polymorphonuclear neutrophils were entrapped in the heart, lungs, and kidneys of cardiopulmonary bypass animals, indicating that cell accumulation may contribute to the developing organ dysfunction.

OriginalsprogEngelsk
TidsskriftCritical Care Medicine
Vol/bind30
Udgave nummer3
Sider (fra-til)670-6
Antal sider7
ISSN0090-3493
DOI
StatusUdgivet - mar. 2002

ID: 243519954