The role of oxygen-derived free radicals in two models of experimental acute pancreatitis: Effects of catalase, superoxide dismutase, dimethylsulfoxide, and allopurinol

1991 ◽  
Vol 69 (21-23) ◽  
pp. 1012-1017 ◽  
Author(s):  
M. L. Steer ◽  
P. L. Rutledge ◽  
R. E. Powers ◽  
M. Saluja ◽  
A. K. Saluja
1984 ◽  
Vol 200 (4) ◽  
pp. 405-413 ◽  
Author(s):  
HILARY SANFEY ◽  
GREGORY B. BULKLEY ◽  
JOHN L. CAMERON

1998 ◽  
Vol 85 (4) ◽  
pp. 1292-1298 ◽  
Author(s):  
William G. Mayhan ◽  
Glenda M. Sharpe

We previously showed [ Am. J. Physiol. 272 ( Heart Circ. Physiol. 41): H2337–H2342, 1997] that nicotine impairs endothelium-dependent arteriolar dilatation. However, mechanisms that accounted for the effect of nicotine on endothelium-dependent vasodilatation were not examined. Thus the goal of this study was to examine the role of oxygen radicals in nicotine-induced impairment of arteriolar reactivity. We measured diameter of cheek pouch resistance arterioles (∼50 μm diameter) in response to endothelium-dependent (ACh and ADP) and -independent (nitroglycerin) agonists before and after infusion of vehicle or nicotine in the absence or presence of superoxide dismutase. ACh, ADP, and nitroglycerin produced dose-related dilatation of cheek pouch arterioles before infusion of vehicle or nicotine. Infusion of vehicle, in the absence or presence of superoxide dismutase (150 U/ml), did not alter endothelium-dependent or -independent arteriolar dilatation. In contrast, infusion of nicotine (2 μg ⋅ kg−1 ⋅ min−1) impaired endothelium-dependent, but not -independent, arteriolar dilatation. In addition, the effect of nicotine on endothelium-dependent vasodilatation was reversed by topical application of superoxide dismutase. We suggest that nicotine impairs endothelium-dependent arteriolar dilatation via an increase in the synthesis/release of oxygen-derived free radicals.


1998 ◽  
Vol 114 ◽  
pp. A442
Author(s):  
J. Bilski ◽  
A. Szlachcic ◽  
J. Jaworek ◽  
M. Cieszkowski ◽  
A. Dembiński ◽  
...  

1989 ◽  
Vol 5 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Toshihiko Koiwai ◽  
Hisao Oguchi ◽  
Shigeyuki Kawa ◽  
Yasutoshi Yanagisawa ◽  
Takeshi Kobayashi ◽  
...  

HPB ◽  
2016 ◽  
Vol 18 ◽  
pp. e324-e325
Author(s):  
P. Miguel ◽  
J. Camelione ◽  
L. Cardozo Bidart ◽  
R. Trapani ◽  
P. Curvale ◽  
...  

2002 ◽  
Vol 11 (6) ◽  
pp. 543-551 ◽  
Author(s):  
Caryl Goodyear-Bruch ◽  
Janet D. Pierce

Oxygen-derived free radicals play an important role in the development of disease in critically ill patients. Normally, oxygen free radicals are neutralized by antioxidants such as vitamin E or enzymes such as superoxide dismutase. However, in patients who require intensive care, oxygen free radicals become a problem when either a decrease in the removal or an overproduction of the radicals occurs. This oxidative stress and the damage due to it have been implicated in many diseases in critically ill patients. Many drugs and treatments now being investigated are directed toward preventing the damage from oxidative stress. The formation of reactive oxygen species, the damage caused by them, and the body’s defense system against them are reviewed. New interventions are described that may be used in critically ill patients to prevent or treat oxidative damage.


2016 ◽  
Vol 50 (12) ◽  
pp. 1350-1360 ◽  
Author(s):  
Fabíula Francisca Abreu ◽  
Ana Carla Araújo Souza ◽  
Simone Aparecida Teixeira ◽  
Antônio Garcia Soares ◽  
Daiane Franco Teixeira ◽  
...  

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