PMID- 7636393
OWN - NLM
STAT- MEDLINE
DCOM- 19950912
LR  - 20131121
IS  - 0022-2143 (Print)
IS  - 0022-2143 (Linking)
VI  - 126
IP  - 2
DP  - 1995 Aug
TI  - Effects of intraperitoneal cyclooxygenase inhibition on inflammatory mediators in 
      dialysate and peritoneal membrane characteristics during peritonitis in 
      continuous ambulatory peritoneal dialysis.
PG  - 204-15
AB  - Peritonitis complicating continuous ambulatory peritoneal dialysis (CAPD) can be 
      used as an in vivo model to study the contribution of mediators in dialysate to 
      the regulation of peritoneal permeability. Previously we reported that changes in 
      the peritoneal appearance rates of the cytokines interleukin-6 (IL-6) and tumor 
      necrosis factor-alpha (TNF alpha) were related to alterations in the effective 
      peritoneal surface area. Changes in the intrinsic peritoneal permeability were 
      mainly related to those in the peritoneal appearance rate of the prostanoid 
      prostaglandin E2 (PGE2) and partly also to that of IL-6. In this intervention 
      study the role of these mediators was further analyzed. Eleven peritonitis 
      episodes were followed on 8 consecutive days from the start of the infection and 
      once after recovery. Indomethacin was given intraperitoneally during the first 3 
      days. beta 2-Microglobulin clearance was used as indicator of the effective 
      peritoneal surface area. The intrinsic peritoneal permeability was characterized 
      functionally by the restriction coefficient. The 15 peritonitis episodes studied 
      previously served as the control group. This study supports the formerly obtained 
      relationships in two ways. First, significant reductions were observed for 
      peritoneal PGE2, 6-keto-PGF1 alpha, and TxB2 during cyclooxygenase inhibition to 
      6%, 0.6%, and 9% of the values on day 1, whereas simultaneously the intrinsic 
      permeability was less increased. This indomethacin effect on intrinsic 
      permeability was not entirely significant, probably because of the additional 
      role of IL-6, which was not influenced by indomethacin. Also, the appearance rate 
      of TNF alpha in the effluent was not affected by cyclooxygenase inhibition. 
      Accordingly, the changes in the effective surface area were similar to those in 
      the control group. Second, in 8 of the 11 cases, new rises both in peritoneal 
      PGE2 and in intrinsic permeability occurred after discontinuation of 
      indomethacin. Rebounds were not seen for TNF alpha or IL-6, and, consistently, 
      not for the effective surface area. In conclusion, local cyclooxygenase 
      inhibition results in a less-increased intrinsic permeability during peritonitis 
      but has no effect on the effective surface area. These data support our previous 
      finding that IL-6 and TNF alpha contribute to alterations in surface area, 
      whereas PGE2 is more involved in intrinsic peritoneal permeability changes.
FAU - Zemel, D
AU  - Zemel D
AD  - Department of Pharmacy, Academic Medical Center, Amsterdam, The Netherlands.
FAU - Struijk, D G
AU  - Struijk DG
FAU - Dinkla, C
AU  - Dinkla C
FAU - Stolk, L M
AU  - Stolk LM
FAU - ten Berge, I J
AU  - ten Berge IJ
FAU - Krediet, R T
AU  - Krediet RT
LA  - eng
PT  - Clinical Trial
PT  - Controlled Clinical Trial
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Lab Clin Med
JT  - The Journal of laboratory and clinical medicine
JID - 0375375
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (beta 2-Microglobulin)
RN  - 54397-85-2 (Thromboxane B2)
RN  - K7Q1JQR04M (Dinoprostone)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Cell Membrane Permeability/physiology
MH  - Dinoprostone/metabolism
MH  - Female
MH  - Humans
MH  - Indomethacin/*therapeutic use
MH  - Interleukin-6/metabolism/physiology
MH  - Male
MH  - Middle Aged
MH  - Peritoneal Dialysis, Continuous Ambulatory/*adverse effects
MH  - Peritoneum/metabolism/pathology/*physiology
MH  - Peritonitis/*drug therapy/*etiology/physiopathology
MH  - Thromboxane B2/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism/physiology
MH  - beta 2-Microglobulin/metabolism
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
PST - ppublish
SO  - J Lab Clin Med. 1995 Aug;126(2):204-15.