PMID- 16523427
OWN - NLM
STAT- MEDLINE
DCOM- 20060816
LR  - 20151119
IS  - 1121-8428 (Print)
IS  - 1121-8428 (Linking)
VI  - 19
IP  - 1
DP  - 2006 Jan-Feb
TI  - Bicarbonate dialysis, unlike acetate-free biofiltration, triggers mediators of 
      inflammation and apoptosis in endothelial and smooth muscle cells.
PG  - 57-64
AB  - BACKGROUND: We previously demonstrated that bicarbonate dialysis solutions 
      incubated with endothelial cells (EC) enhance nitric oxide synthase (NOS). We 
      then investigated whether blood circulated in simulated dialysis circuits 
      triggers inflammatory and apoptotic mediators in vessel wall cells, aiming to 
      compare the effects of bicarbonate hemodialysis (BHD) and acetate-free 
      biofiltration (AFB). METHODS: Blood units from 22 healthy donors were dialyzed on 
      AN69 with BHD in 11 sessions and AFB in another 11 sessions. Each dialysate 
      remained endotoxin-free during the 60 min of dialysis. Blood samples having been 
      re-circulated for 15 and 60 min were incubated with EC and smooth muscle cells 
      (SMC), which were then investigated for NOS activity (3H citrulline production 
      from 3H arginine), mRNAs transcription of the inducible isoforms of NOS (iNOS) 
      and cyclooxygenase (COX-2) and the pro-apoptotic p53 protein. To investigate 
      cell-cell interactions, in an-other series of 16 simulated dialyses, 
      lympho-monocytes from blood circulated in either BHD or AFB were incubated with 
      EC co-cultured in transwell devices with SMC. NOS activity was measured in EC and 
      SMC. RESULTS: In comparison to AFB, blood circulated in BHD induced a 
      significantly greater enhancement of NOS activity in EC, SMC and mRNAs 
      transcription of pro-inflammatory iNOS, COX-2 and pro-apoptotic p53 (for each BHD 
      data series p < 0.01 to p < 0.0001 vs. AFB). Lympho-monocytes from blood 
      circulated in BHD but not in AFB, triggered the final SMC activation. 
      CONCLUSIONS: Ex vivo AFB is less effective than BHD in activating vessel wall 
      cells to synthesis/release of pro-inflammatory and pro-apoptotic mediators.
FAU - Amore, Alessandro
AU  - Amore A
AD  - Nephrology, Dialysis and Transplantation Unit, Regina Margherita Hospital, Turin, 
      Italy.
FAU - Cirina, Paola
AU  - Cirina P
FAU - Bonaudo, Roberto
AU  - Bonaudo R
FAU - Conti, Giuvanni
AU  - Conti G
FAU - Chiesa, Monica
AU  - Chiesa M
FAU - Coppo, Rossanna
AU  - Coppo R
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - J Nephrol
JT  - Journal of nephrology
JID - 9012268
RN  - 0 (Bicarbonates)
RN  - 0 (Biomarkers)
RN  - 0 (Dialysis Solutions)
RN  - 0 (Membrane Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
SB  - IM
MH  - Apoptosis/*drug effects
MH  - Bicarbonates/*adverse effects
MH  - Biomarkers/metabolism
MH  - Cells, Cultured
MH  - Cyclooxygenase 2/genetics/metabolism
MH  - Dialysis Solutions/*adverse effects
MH  - Endothelium, Vascular/metabolism/*pathology
MH  - Gene Expression
MH  - *Hemodiafiltration
MH  - Humans
MH  - In Vitro Techniques
MH  - Inflammation/etiology/metabolism/*pathology
MH  - Membrane Proteins/genetics/metabolism
MH  - Muscle, Smooth, Vascular/metabolism/*pathology
MH  - Nitric Oxide Synthase/genetics/metabolism
MH  - RNA, Messenger/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Suppressor Protein p53/genetics/metabolism
EDAT- 2006/03/09 09:00
MHDA- 2006/08/17 09:00
CRDT- 2006/03/09 09:00
PHST- 2006/03/09 09:00 [pubmed]
PHST- 2006/08/17 09:00 [medline]
PHST- 2006/03/09 09:00 [entrez]
PST - ppublish
SO  - J Nephrol. 2006 Jan-Feb;19(1):57-64.