scholarly journals Modulation of Sulfur Mustard Toxicity by Arginine Analogues and Related Nitric Oxide Synthase Inhibitors in Vitro

1998 ◽  
Vol 46 (1) ◽  
pp. 112-123 ◽  
Author(s):  
Thomas W. Sawyer
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Sulfur Mustard ◽  
Nitric Oxide Synthase Inhibitors ◽  
Oxide Synthase

Nitric oxide synthase inhibitors 7- and 6-nitroindazole relax smooth muscle in vitro

1994 ◽  
Vol 256 (1) ◽  
pp. R5-R6 ◽  
Author(s):  
Andrew D. Medhurst ◽  
Carol Greenlees ◽  
Andrew A. Parsons ◽  
Susan J. Smith
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitors ◽  
Oxide Synthase

scholarly journals Nitric Oxide Synthase Gene Transfer Overcomes the Inhibition of Wound Healing by Sulfur Mustard in a Human Keratinocyte In Vitro Model

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Hiroshi Ishida ◽  
Radharaman Ray ◽  
Jack Amnuaysirikul ◽  
Keiko Ishida ◽  
Prabhati Ray
Keyword(s):  
Nitric Oxide ◽  
Wound Healing ◽  
Nitric Oxide Synthase ◽  
Gene Transfer ◽  
Sulfur Mustard ◽  
No Production ◽  
Skin Injury ◽  
Inos Gene ◽  
Oxide Synthase

Sulfur mustard (SM) is a chemical warfare agent that causes extensive skin injury. Previously we reported that SM exposure resulted in suppression of inducible nitric oxide synthase (iNOS) expression to inhibit the healing of scratch wounds in a cultured normal human epidermal keratinocyte (NHEK) model. Based on this finding, the present study was to use adenovirus-mediated gene transfer of iNOS to restore the nitric oxide (NO) supply depleted by exposure to SM and to evaluate the effect of NO on wound healing inhibited by SM in NHEKs. The effect of the iNOS gene transfer on iNOS protein expression and NO generation were monitored by Western blot and flow cytometry, respectively. Wound healing with or without the iNOS gene transfer after SM exposure was assessed by light and confocal microscopy. The iNOS gene transfer via adenovirus resulted in overexpression of the iNOS and an increase in NO production regardless of SM exposure in the NHEK model. The gene transfer was also effective in overcoming the inhibition of wound healing due to SM exposure leading to the promotion of wound closure. The findings in this study suggest that the iNOS gene transfer is a promising therapeutic strategy for SM-induced skin injury.

Nitric oxide synthase inhibitors modulate lipopolysaccharide-induced hepatocyte injury: dissociation between in vivo and in vitro effects

2003 ◽  
Vol 3 (12) ◽  
pp. 1627-1638 ◽  
Author(s):  
Hassan Farghali ◽  
Nikolina Canová ◽  
Tomáš Kučera ◽  
Jindřich Martı́nek ◽  
Karel Mašek
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitors ◽  
Hepatocyte Injury ◽  
In Vitro Effects ◽  
Oxide Synthase

scholarly journals Modulation of glomerular arteriolar tone by nitric oxide synthase inhibitors.

1993 ◽  
Vol 4 (5) ◽  
pp. 1127-1132
Author(s):  
R M Edwards ◽  
W Trizna
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inhibitory Effect ◽  
Lumen Diameter ◽  
Nitric Oxide Synthase Inhibitors ◽  
Afferent Arterioles ◽  
Arteriolar Tone ◽  
Oxide Synthase

The inhibition of nitric oxide production has been shown to reduce RBF. The effects of the nitric oxide synthase inhibitors, N omega-nitro-L-arginine and NG-monomethyl-L-arginine, on afferent and efferent arterioles isolated from rabbit kidneys were examined. Under basal conditions, N omega-nitro-L-arginine (10(-7) to 10(-3) M) had no effect on efferent arteriole lumen diameter but caused a 40% decrease in the lumen diameter of afferent arterioles. In afferent and efferent arterioles precontracted with norepinephrine, N omega-nitro-L-arginine and NG-monomethyl-L-arginine (3 x 10(-4) M) markedly attenuated the vasorelaxant effects of the endothelium-dependent vasodilator acetylcholine. In both arterioles, the inhibitory effect of N omega-nitro-L-arginine on acetylcholine-induced relaxation could be reversed by L- but not D-arginine (10(-3) M). However, N omega-nitro-L-arginine had no effect on the relaxation produced by the endothelium-independent vasodilators prostaglandin E2 (afferent) and dopamine (efferent). These observations demonstrate that under the in vitro conditions used in this study, afferent arterioles but not efferent arterioles synthesize and release nitric oxide in the basal state. However, both arterioles release nitric oxide in response to an endothelium-dependent vasodilator. The results of this study provide further evidence for an important role of nitric oxide in the regulation of renal hemodynamics.

Nitric oxide synthase inhibitors attenuate human monocyte chemotaxis in vitro

1993 ◽  
Vol 53 (5) ◽  
pp. 498-503 ◽  
Author(s):  
Sergei N. Belenky ◽  
Richard A. Robbins ◽  
Israel Rubinstein
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Human Monocyte ◽  
Nitric Oxide Synthase Inhibitors ◽  
Monocyte Chemotaxis ◽  
Oxide Synthase

Hippocampal in vitro kindling is not blocked by nitric oxide synthase inhibitors

Neuroreport ◽  
1994 ◽  
Vol 5 (9) ◽  
pp. 1102-1104 ◽  
Author(s):  
Sonja Yvette Grooms ◽  
Leslie Sargent Jones
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitors ◽  
Oxide Synthase
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