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Related Experiment Videos

Cardiopulmonary bypass primes polymorphonuclear leukocytes

J D Schwartz1, P Shamamian, D S Schwartz

  • 1Department of Surgery, New York University Medical Center, New York 10016, USA.

The Journal of Surgical Research
|July 9, 1998
PubMed
Summary

Cardiopulmonary bypass (CPB) primes polymorphonuclear leukocytes (PMNs), increasing their superoxide production. This primed PMN state correlates with elevated inflammatory mediators, potentially contributing to organ injury after CPB.

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Area of Science:

  • Immunology
  • Cardiovascular Surgery
  • Critical Care Medicine

Background:

  • Polymorphonuclear leukocyte (PMN) superoxide production is linked to cardiopulmonary bypass (CPB)-related organ injury.
  • PMN priming, an enhanced response to a secondary stimulus, is a potential mechanism for this injury.

Purpose of the Study:

  • To investigate if PMN priming occurs during CPB.
  • To determine if PMN priming is temporally related to plasma levels of complement C3a, IL-6, and IL-8.

Main Methods:

  • Isolated PMNs from 10 CPB patients at various time points: pre-bypass, post-protamine, and 6/24 hours post-CPB.
  • Measured PMN superoxide production using cytochrome c reduction assay, with and without priming (platelet-activating factor) and activation (PMA or FMLP).
  • Quantified plasma levels of C3a, IL-6, and IL-8 via enzyme-linked immunosorbent assay.

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Main Results:

  • PMA-activated PMN superoxide production was significantly elevated 6 hours post-CPB, indicating in vivo PMN priming.
  • CPB potentiated in vitro PMN priming by platelet-activating factor.
  • Plasma levels of C3a increased at protamine administration, while IL-6 and IL-8 rose at 6 hours post-CPB.

Conclusions:

  • CPB directly primes PMNs and enhances their priming response to platelet-activating factor.
  • The primed PMN state coincides with increased inflammatory mediators.
  • This suggests a mechanism for CPB-induced organ dysfunction.