Compounds > 1-1-diethyl-2-hydroxy-2-nitrosohydrazine

1-1-diethyl-2-hydroxy-2-nitrosohydrazine and Hyperemia

1-1-diethyl-2-hydroxy-2-nitrosohydrazine has been researched along with Hyperemia* in 1 studies

Other Studies

1 other study(ies) available for 1-1-diethyl-2-hydroxy-2-nitrosohydrazine and Hyperemia

Article	Year
Endotoxin augments cerebral hyperemic response to halothane by inducing nitric oxide synthase and cyclooxygenase. Anesthesia and analgesia, 2000, Volume: 91, Issue:4 We examined the cerebral hyperemic response to halothane after treatment with bacterial lipopolysaccharide (LPS). To determine the involvement of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2), we tested whether the effect of LPS on halothane-induced hyperemia was altered by pretreatment with the selective iNOS inhibitor, aminoguanidine (100 mg/kg), COX-2 inhibitor, NS-398 (5 mg/kg), or enzyme expression inhibitor, dexamethasone (4 mg/kg). Further, we examined whether the administration of a nitric oxide donor, diethylamine NONOate, would change the cerebral hyperemic response of halothane. Sprague-Dawley rats were anesthetized with 0.5 minimum alveolar anesthetic concentration of halothane and artificially ventilated. Regional cerebrocortical blood flow (rCBF) was assessed by laser-Doppler flowmetry. LPS (1 mg/kg) was administered intracerebroventricularly; artificial cerebrospinal fluid was used in controls. Four hours after LPS infusion, iNOS and COX-2 messenger ribonucleic acid (mRNA) levels (reverse transcription-polymerase chain reaction) and enzyme activities (arginine-citrulline conversion and prostaglandin E(2) enzyme immunoassay) were significantly increased. LPS enhanced halothane-induced 3.9 and 1.6-fold increases in rCBF at 1.0 and 1.5 minimum alveolar concentration, respectively. Co-treatment with NS-398 attenuated, but aminoguanidine or dexamethasone abolished the effect of LPS on halothane-induced rCBF increase. Diethylamine NONOate mimicked the enhanced rCBF response to halothane. These results suggest that LPS augmented halothane-induced cerebrocortical hyperemia by induction of iNOS and COX-2. Topics: Anesthetics, Inhalation; Animals; Arginine; Cerebrovascular Circulation; Citrulline; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dexamethasone; Dinoprostone; Endotoxins; Enzyme Inhibitors; Escherichia coli; Guanidines; Halothane; Hydrazines; Hyperemia; Isoenzymes; Laser-Doppler Flowmetry; Lipopolysaccharides; Male; Nitric Oxide Donors; Nitric Oxide Synthase; Nitrobenzenes; Nitrogen Oxides; Peroxidases; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Sprague-Dawley; Respiration, Artificial; Sulfonamides	2000

Article

Year

Endotoxin augments cerebral hyperemic response to halothane by inducing nitric oxide synthase and cyclooxygenase.

Anesthesia and analgesia, 2000, Volume: 91, Issue:4

We examined the cerebral hyperemic response to halothane after treatment with bacterial lipopolysaccharide (LPS). To determine the involvement of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2), we tested whether the effect of LPS on halothane-induced hyperemia was altered by pretreatment with the selective iNOS inhibitor, aminoguanidine (100 mg/kg), COX-2 inhibitor, NS-398 (5 mg/kg), or enzyme expression inhibitor, dexamethasone (4 mg/kg). Further, we examined whether the administration of a nitric oxide donor, diethylamine NONOate, would change the cerebral hyperemic response of halothane. Sprague-Dawley rats were anesthetized with 0.5 minimum alveolar anesthetic concentration of halothane and artificially ventilated. Regional cerebrocortical blood flow (rCBF) was assessed by laser-Doppler flowmetry. LPS (1 mg/kg) was administered intracerebroventricularly; artificial cerebrospinal fluid was used in controls. Four hours after LPS infusion, iNOS and COX-2 messenger ribonucleic acid (mRNA) levels (reverse transcription-polymerase chain reaction) and enzyme activities (arginine-citrulline conversion and prostaglandin E(2) enzyme immunoassay) were significantly increased. LPS enhanced halothane-induced 3.9 and 1.6-fold increases in rCBF at 1.0 and 1.5 minimum alveolar concentration, respectively. Co-treatment with NS-398 attenuated, but aminoguanidine or dexamethasone abolished the effect of LPS on halothane-induced rCBF increase. Diethylamine NONOate mimicked the enhanced rCBF response to halothane. These results suggest that LPS augmented halothane-induced cerebrocortical hyperemia by induction of iNOS and COX-2.

Topics: Anesthetics, Inhalation; Animals; Arginine; Cerebrovascular Circulation; Citrulline; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dexamethasone; Dinoprostone; Endotoxins; Enzyme Inhibitors; Escherichia coli; Guanidines; Halothane; Hydrazines; Hyperemia; Isoenzymes; Laser-Doppler Flowmetry; Lipopolysaccharides; Male; Nitric Oxide Donors; Nitric Oxide Synthase; Nitrobenzenes; Nitrogen Oxides; Peroxidases; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Sprague-Dawley; Respiration, Artificial; Sulfonamides

2000