Eicosanoid Release as an Indicator of Membrane Biocompatibility

Author(s):  
Georg Schultze ◽  
Karl Wagner ◽  
Hans-Helmut Neumayer ◽  
Martin Molzahn
Keyword(s):  
1999 ◽  
Vol 14 (Suppl_3) ◽  
pp. 269-269
Author(s):  
A. Lanzone ◽  
E. Pierro ◽  
F. Minici ◽  
C.L. Andreani ◽  
F. Miceli ◽  
...  

1997 ◽  
Vol 83 (2) ◽  
pp. 530-536 ◽  
Author(s):  
Patricia Rothenbach ◽  
Richard H. Turnage ◽  
Jose Iglesias ◽  
Angela Riva ◽  
Lori Bartula ◽  
...  

Rothenbach, Patricia, Richard H. Turnage, Jose Iglesias, Angela Riva, Lori Bartula, and Stuart I. Myers. Downstream effects of splanchnic ischemia-reperfusion injury on renal function and eicosanoid release. J. Appl. Physiol.82(2): 530–536, 1997.—This study examines the hypothesis that intestinal ischemia-reperfusion (I/R) injury contributes to renal dysfunction by altered renal eicosanoid release. Anesthetized Sprague-Dawley rats underwent 60 min of sham or superior mesenteric artery (SMA) occlusion with 60 min of reperfusion. The I/R groups received either allopurinol, pentoxifylline, 1-benzylimidazole, or carrier before SMA occlusion. In vivo renal artery blood flow was measured by Transonic flow probes, the kidneys were then perfused in vitro for 30 min, and the effluent was analyzed for eicosanoid release and renal function. Intestinal I/R caused a twofold increase in the ratio of renal release of thromboxane B2to prostaglandin E2and to 6-ketoprostaglandin F1αcompared with the sham level, with a corresponding 25% decrease in renal sodium and inulin clearance and renal blood flow. Pentoxifylline or allopurinol pretreatment restored renal eicosanoid release and renal sodium and inulin clearance to the sham level but did not alter renal blood flow. Pretreatment with 1-benzylimidazole restored renal function, eicosanoid release, and renal blood flow to sham levels. These data suggest that severe intestinal I/R contributes to the downregulation of renal function. The decrease in renal function is due in part to toxic oxygen metabolites, which occur in the milieu of altered renal eicosanoid release, reflecting a decrease in vasodilator and an increase in vasoconstrictor eicosanoids.


1988 ◽  
Vol 1 (2) ◽  
pp. 109-114
Author(s):  
G. R. Elliott ◽  
A. P. M. Lauwen ◽  
I. L. Bonta

Dibutyryl cytidine and adenosine 3':5'-cyclic monophosphates (db-cCMP and db-cAMP respectively) inhibited the synthesis of thromboxane (TX) B2, the stable product of TXA2, and leukotriene (LT) B4 by 4-day carrageenin-elicited rat peritoneal macrophages stimulated by the calcium ionophore A23187. Incubation of macrophages with dbcAMP, at concentrations inhibiting eicosanoid release, was associated with an increase in intracellular cAMP concentrations. No such increase was seen when db-cCMP was used.


2011 ◽  
Vol 13 (4) ◽  
pp. R123 ◽  
Author(s):  
Janny C de Grauw ◽  
Chris HA van de Lest ◽  
Paul van Weeren

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