PMID- 8938277
OWN - NLM
STAT- MEDLINE
DCOM- 19970108
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 27 Suppl 1
DP  - 1996
TI  - Initiation of white cell activation during cardiopulmonary bypass: cytokines and 
      receptors.
PG  - S1-5
AB  - The pathogenesis of organ injury induced by extracorporeal circulation involves 
      many inflammatory cascades and cellular components of the immune system. One 
      therapeutic approach is to target the neutrophil and minimize the deleterious 
      effects of neutrophil activation during bypass. Mechanical removal of circulating 
      neutrophils from the perfusate by filtration produced profound leukopenia in a 
      dog model that persisted for 8-12 h post-bypass. The leukocyte-depleted animals 
      had less lung sequestration of white cells than control animals and less evidence 
      of white-cell activation. These differences resulted in significantly improved 
      pulmonary gas exchange in the post-bypass period. Another approach to reducing 
      cardiopulmonary bypass (CPB) neutrophil-mediated injury is modulation of 
      neutrophil-endothelial adherence. One strategy is to improve the biocompatibility 
      of the bypass circuit. Our laboratory measured the upregulation of the 
      neutrophil-adhesion molecules CD11b and CD18 during CPB but did not demonstrate 
      significant differences between membrane and bubble oxygenators. However, studies 
      in pigs undergoing CPB with a standard extracorporeal circuit or a heparin-coated 
      CPB circuit found less pulmonary injury in the heparin-coated group of animals. 
      Specific therapy to inhibit adhesion molecule expression using the 
      anti-inflammatory compound NPC 15669 has shown promise. Marked inhibition of 
      neutrophil CD18 expression during and post-bypass, better gas exchange, and lower 
      pulmonary vascular resistance occurred in the treated animals. The role of 
      cytokines in relation to the morbidity associated with bypass is not clearly 
      defined. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), IL-6, and 
      IL-8 are usually (but not uniformly) elevated after cardiac operations.
FAU - Cameron, D
AU  - Cameron D
AD  - Department of Surgery, Johns Hopkins Hospital, Baltimore, Maryland, USA.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Cytokines)
RN  - 0 (Integrins)
SB  - IM
MH  - Animals
MH  - Cardiopulmonary Bypass/*adverse effects
MH  - Cytokines/*physiology
MH  - Humans
MH  - Integrins/*physiology
MH  - Leukocytes/*physiology
MH  - Neutrophil Activation/*physiology
RF  - 12
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
AID - 10.1097/00005344-199600001-00004 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1996;27 Suppl 1:S1-5. doi: 
      10.1097/00005344-199600001-00004.