Exacerbation of experimental colitis by nonsteroidal anti-inflammatory drugs is not related to elevated leukotriene B4 synthesis.

@article{Wallace1992ExacerbationOE,
  title={Exacerbation of experimental colitis by nonsteroidal anti-inflammatory drugs is not related to elevated leukotriene B4 synthesis.},
  author={John L Wallace and Catherine M. Keenan and Danielle Gale and T. Scott Shoupe},
  journal={Gastroenterology},
  year={1992},
  volume={102 1},
  pages={18-27}
}
The ability of nonsteroidal anti-inflammatory drugs to exacerbate experimental colitis, and the possible contributions of the "shunting" of arachidonate via the 5-lipoxygenase pathway, were investigated using a rat model in which colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid in a vehicle of 50% ethanol. Twice daily treatment with indomethacin (0.1-1 mg/kg SC) during the first week after trinitrobenzene sulfonic acid/ethanol administration resulted in dose… CONTINUE READING

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In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
These results suggest that inhibitors of colonic prostaglandin synthesis can markedly exacerbate colitis , and that this effect is unrelated to alterations in colonic leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
These results suggest that inhibitors of colonic prostaglandin synthesis can markedly exacerbate colitis , and that this effect is unrelated to alterations in colonic leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
In in vitro studies using samples of inflamed colon and in vivo studies in which colonic eicosanoid production was measured by colonic dialysis , inhibition of prostaglandin E2 synthesis was not accompanied by significant changes in leukotriene B4 synthesis .
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