1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole has been researched along with Endotoxemia* in 2 studies
2 other study(ies) available for 1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole and Endotoxemia
| Article | Year |
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Carboxy-PTIO, a scavenger of nitric oxide, selectively inhibits the increase in medullary perfusion and improves renal function in endotoxemia.
The acute renal failure associated with septic shock is associated with a high mortality despite dialytic therapies. Endotoxemia leads to marked changes in the distribution of intrarenal perfusion that may be independent of alterations in total renal blood flow or systemic hemodynamics. Modulation of this intrarenal redistribution may protect against acute renal failure. This study examines the effect of carboxy-2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO), a scavenger of nitric oxide (NO), on systemic and intrarenal hemodynamics measured by laser Doppler flowmetry following the induction of endotoxemia in the anesthetized rat. Infusion of lipopolysaccharide (LPS) led to a prompt reduction in inulin clearance at 60 min, which remained reduced for 6 h in saline-treated rats. Administration of carboxy-PTIO led to a sustained increase in inulin clearance over 360 min post-LPS. During endotoxemia, cortical perfusion fell acutely by 29 +/- 8%, whereas medullary perfusion increased by 71 +/- 11%. The increase in medullary perfusion was potently and selectively inhibited by carboxy-PTIO. We propose that inhibition of medullary hyperemia maintains glomerular hydrostatic pressure, thus leading to the improved renal function during endotoxemia and that scavenging of NO may prove to be a useful therapeutic option in the acute renal failure associated with septic shock. Topics: Animals; Benzoates; Endotoxemia; Hemodynamics; Imidazoles; Insulin; Kidney; Lipopolysaccharides; Male; Nitric Oxide; Perfusion; Rats; Rats, Wistar; Renal Circulation | 2002 |
Effect of an imidazolineoxyl nitric oxide on prostaglandin synthesis in experimental shock: possible role of nitrogen dioxide in prostacyclin synthase inactivation.
The effect of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a nitric oxide (NO) scavenger that yields nitrogen dioxide (NO(2)) in a rat endotoxemia model was investigated. Endotoxin (lipopolysaccharide [LPS]) increased NO synthase (NOS) activity and inducible NOS expression measured in lung and plasma levels of nitrite/nitrate, 6-oxo-prostaglandin (PG) F(1alpha), thromboxane B(2), and PGF(2alpha). Infusion of cPTIO significantly reduced LPS-induced mean arterial blood pressure decline and mortality and selectively reduced LPS-induced 6-oxo-PGF(1alpha) plasma levels and prostacyclin synthase (PGIS) activity measured in the lung and aorta. In vitro, PGIS activity in aorta rings was not modified by SNAP (NO donor), cPTIO slightly inhibited the enzyme but not in the presence of L-N(G)-monomethyl arginine, and SNAP in combination with cPTIO significantly inhibited PGIS. Thus, cPTIO may be beneficial in endotoxic shock because of NO scavenging and PGIS inactivation, which could be mediated by NO(2). Topics: 6-Ketoprostaglandin F1 alpha; Animals; Aorta; Benzoates; Culture Techniques; Cytochrome P-450 Enzyme Inhibitors; Cytochrome P-450 Enzyme System; Endotoxemia; Imidazoles; Intramolecular Oxidoreductases; Lipopolysaccharides; Lung; Male; Nitrates; Nitric Oxide Synthase; Nitrites; Nitrogen Dioxide; Prostaglandins; Rats; Rats, Sprague-Dawley | 2001 |