PMID- 19882198
OWN - NLM
STAT- MEDLINE
DCOM- 20100330
LR  - 20131121
IS  - 1496-8975 (Electronic)
IS  - 0832-610X (Linking)
VI  - 57
IP  - 1
DP  - 2010 Jan
TI  - Persistency and pathway of isoflurane-induced inhibition of superoxide production 
      by neutrophils.
PG  - 50-7
LID - 10.1007/s12630-009-9205-8 [doi]
AB  - BACKGROUND: Our previous work has demonstrated that treatment with isoflurane has 
      a preconditioning-like inhibitory effect on superoxide production (SOP) by 
      polymorphonuclear neutrophils. The current objectives were to determine 
      persistency of this effect and to clarify where in the signalling pathway this 
      inhibition of SOP occurred. The latter was accomplished using two 
      receptor-dependent neutrophil agonists, platelet activating factor (PAF) and 
      formyl-methionyl-leucyl-phenylalanine (fMLP), and two receptor-independent 
      neutrophil stimuli, the protein-kinase C stimulator, phorbol myristate acetate 
      (PMA), and the calcium ionophore, A23187. METHODS: Arterial blood samples were 
      obtained from eight dogs under baseline condition (conscious state), during 
      isoflurane (1 MAC) administration, and 24 and 48 hr post-isoflurane (also in 
      conscious state). Neutrophils were isolated and stimulated with 1 muM 
      concentrations of PAF, fMLP, PMA, and A23187. SOP was measured 
      spectrophotometrically. RESULTS: Isoflurane administration caused (1) an 
      approximate 50% decrease in SOP during PAF or fMLP (P < 0.01 vs baseline), which 
      remained evident from 24 to 48 hr following isoflurane; (2) an initial 29% 
      decrease in SOP during PMA (P < 0.05 vs baseline), which returned to baseline by 
      24 hr following isoflurane; and (3) no change in SOP during A23187 (P > 0.05 vs 
      baseline). CONCLUSIONS: Isoflurane administration caused prolonged (from 24 to 48 
      hr) decreases in agonist-induced SOP by neutrophils. This effect involved 
      inhibition at site(s) in the signalling pathway upstream from protein kinase C. 
      The current findings suggest that the intraoperative use of isoflurane may result 
      in an extended impairment to the antibacterial host defense mechanism and that 
      neutrophil inhibition may play a role in the delayed tissue protection afforded 
      by treatment with volatile anesthetics.
FAU - Saad, Maged M
AU  - Saad MM
AD  - Section of Cardiology, Advocate Illinois Masonic Medical Center, Chicago, IL, 
      USA.
FAU - Eom, Woosik
AU  - Eom W
FAU - Hu, Guochang
AU  - Hu G
FAU - Kim, Song-Jung
AU  - Kim SJ
FAU - Crystal, George J
AU  - Crystal GJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091031
PL  - United States
TA  - Can J Anaesth
JT  - Canadian journal of anaesthesia = Journal canadien d'anesthesie
JID - 8701709
RN  - 0 (Anesthetics, Inhalation)
RN  - 0 (Platelet Activating Factor)
RN  - 11062-77-4 (Superoxides)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - CYS9AKD70P (Isoflurane)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Anesthetics, Inhalation/*pharmacology/toxicity
MH  - Animals
MH  - Calcimycin/pharmacology
MH  - Dogs
MH  - Isoflurane/*pharmacology/toxicity
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Neutrophils/*drug effects/metabolism
MH  - Platelet Activating Factor/pharmacology
MH  - Protein Kinase C/metabolism
MH  - Signal Transduction/drug effects
MH  - Spectrophotometry
MH  - Superoxides/*metabolism
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Time Factors
EDAT- 2009/11/03 06:00
MHDA- 2010/03/31 06:00
CRDT- 2009/11/03 06:00
PHST- 2009/07/21 00:00 [received]
PHST- 2009/10/01 00:00 [accepted]
PHST- 2009/11/03 06:00 [entrez]
PHST- 2009/11/03 06:00 [pubmed]
PHST- 2010/03/31 06:00 [medline]
AID - 10.1007/s12630-009-9205-8 [doi]
PST - ppublish
SO  - Can J Anaesth. 2010 Jan;57(1):50-7. doi: 10.1007/s12630-009-9205-8. Epub 2009 Oct 
      31.