1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole and Shock--Septic

1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole has been researched along with Shock--Septic* in 3 studies

Reviews

1 review(s) available for 1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole and Shock--Septic

ArticleYear
A new nitric oxide scavenger, imidazolineoxyl N-oxide derivative, and its effects in pathophysiology and microbiology.
    Current topics in microbiology and immunology, 1995, Volume: 196

    Topics: Amino Acid Oxidoreductases; Animals; Aorta; Arginine; Benzoates; Capillary Permeability; Cyclic N-Oxides; Hypotension; Imidazoles; In Vitro Techniques; Neoplasms, Experimental; Nitric Oxide; Nitric Oxide Synthase; Rabbits; Rats; Shock, Septic; Vasodilator Agents

1995

Other Studies

2 other study(ies) available for 1-3-dihydroxy-4-4-5-5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole and Shock--Septic

ArticleYear
Effects of carboxy-PTIO on systemic hemodynamics, liver energetics, and concentration of liver metabolites during endotoxic shock in rabbits: a 31P and 1H magnetic resonance spectroscopic study.
    Critical care medicine, 1997, Volume: 25, Issue:6

    To investigate the effects of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (carboxy-PTIO), a nitric oxide scavenger, on the lipopolysaccharide-induced hypotension, hepatocellular dysfunction, and liver damage in endotoxic rabbits.. Experimental, comparative study.. Laboratory of a university hospital.. Eighteen Japanese white rabbits (3.0 to 3.2 kg body weight) anesthetized with ketamine-xylazine were studied.. We randomly divided the rabbits into three groups: saline controls (group 1, n = 5); animals receiving lipopolysaccharide (400 micrograms/kg) alone (group 2, n = 8); and animals receiving lipopolysaccharide plus carboxy-PTIO at a rate of 0.17 mg/kg/min for 3 hrs (group 3, n = 5). Blood gases and mean arterial pressure (MAP) were monitored. In vivo phosphorus-31 magnetic resonance spectra were continuously obtained every 30 mins. In addition, the livers were sampled and underwent fractionation at 7 hrs after lipopolysaccharide administration. The hydrophilic and hydrophobic extracts from the livers were analyzed by in vitro hydrogen-1 and phosphorus-31 magnetic resonance spectroscopy.. After the administration of lipopolysaccharide, the first phase of decrease in MAP within 30 mins was followed by partial recovery within the next 30 mins. In group 2, MAP started to decrease progressively within 180 mins after lipopolysaccharide administration (second phase) and decreased by 33% from the baseline value to 49 +/- 9 mm Hg at 420 mins. In contrast, the infusion of carboxy-PTIO significantly attenuated the second decrease in MAP (68 +/- 10 mm Hg, at 420 mins). In group 2, a slow and progressive decrease in adenosine triphosphate (ATP) and increase in inorganic phosphate concentrations occurred from 120 mins after lipopolysaccharide administration, and continued throughout the observation period. These changes were accompanied by a progressive decrease in intracellular pH. On the other hand, in group 3, there were no significant changes in ATP and inorganic phosphate concentrations compared with the controls from 120 to 360 mins after lipopolysaccharide administration. Moreover, restorations of both arterial and hepatocellular acidosis were observed in group 3. The differences of the degree of liver damage--as determined by the total amount of phospholipid, free fatty acids concentration, and membrane fluidity--were not significant among the three groups. Three of eight rabbits in group 2 died within 7 hrs, but no animal in the other two groups died during the study.. The results of this study indicate that the infusion of carboxy-PTIO: a) prevented the delayed hypotension associated with endotoxic shock in rabbits; b) returned the hepatocellular ATP concentrations nearly to the level of the controls and alleviated hepatocellular acidosis; c) normalized various hydrophilic metabolites, such as lactate and alanine in the liver; and d) did not exacerbate liver injury after the administration of lipopolysaccharide. These findings indicate that carboxy-PTIO, a nitric oxide scavenger, may have a positive vasopressor effect during hypodynamic septic shock without exacerbating liver injury.

    Topics: Acidosis; Adenosine Triphosphate; Animals; Benzoates; Blood Pressure; Free Radical Scavengers; Hydrogen; Hypotension; Imidazoles; Lipopolysaccharides; Liver; Magnetic Resonance Spectroscopy; Nitric Oxide; Phosphates; Phosphorus Radioisotopes; Rabbits; Shock, Septic

1997
Therapeutic effects of imidazolineoxyl N-oxide against endotoxin shock through its direct nitric oxide-scavenging activity.
    Biochemical and biophysical research communications, 1994, Jul-29, Volume: 202, Issue:2

    We recently found a new class of nitric oxide (NO) antidote, i.e., 2-phenyl-4,4,5,5,-tetramethylimidazoline-1-oxyl-3-oxide derivatives (PTIOs). It has a potent inhibitory action against endothelium-derived relaxing factor. Here, we report the effect of a water-soluble carboxy derivative of PTIO (carboxy-PTIO) on endotoxin shock. Endotoxin [lipopolysaccharide (LPS)] (10 mg/kg) was injected into Wistar rats, and the mean arterial blood pressure (MABP), heart rate and urinary parameters were continuously measured. The MABP and urine volume gradually decreased during 1 hr after LPS injection, and within 4 hr, both values decreased to 50-70%. When carboxy-PTIO at 0.056-1.70 mg/kg/min was infused for 1 hr beginning 90 min after the LPS injection, the hypotension, renal dysfunction and survival rate were much improved and the state of shock was avoided. Carboxy-PTIO administered to normal rats did not affect each parameter. Measurement of urinary output of carboxy-PTIO and carboxy-2-phenyl-4,4,5,5-tetramethylimidazole-1-oxyl (carboxy-PTI), which is a reaction product of carboxy-PTIO and NO, showed that conversion of carboxy-PTIO to carboxy-PTI was augmented by LPS treatment due to the increased production of NO, and that the enhanced conversion (PTIO-->PTI) was significantly inhibited by administration of N omega-monomethyl-L-arginine. This indicates that carboxy-PTIO exhibits a potent therapeutic value in endotoxin shock through the direct scavenging action against NO.

    Topics: Animals; Benzoates; Blood Pressure; Cyclic N-Oxides; Escherichia coli; Free Radical Scavengers; Heart Rate; Imidazoles; Kidney; Lipopolysaccharides; Male; Nitric Oxide; Rats; Rats, Wistar; Shock, Septic; Urine

1994