Effects of nitric oxide donor and inhibitor on prostaglandin E2-like activity, malondialdehyde and reduced glutathione levels after skeletal muscle ischemia-reperfusion

2001 ◽  
Vol 65 (4) ◽  
pp. 179-183 ◽  
Author(s):  
H. Sayan ◽  
A. Babül ◽  
B. Ugurlu
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Prostaglandin E2 ◽  
Reduced Glutathione ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Muscle Ischemia

Nitric Oxide Synthase-Independent Generation of Nitric Oxide in Rat Skeletal Muscle Ischemia-Reperfusion Injury

Nitric Oxide ◽  
1999 ◽  
Vol 3 (1) ◽  
pp. 75-84 ◽  
Author(s):  
D.A. Lepore ◽  
A.V. Kozlov ◽  
A.G. Stewart ◽  
J.V. Hurley ◽  
W.A. Morrison ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Rat Skeletal Muscle ◽  
Muscle Ischemia ◽  
Oxide Synthase

The effect of the nitric oxide donor sodium nitroprusside on glucose uptake in human primary skeletal muscle cells

Nitric Oxide ◽  
2009 ◽  
Vol 21 (2) ◽  
pp. 126-131 ◽  
Author(s):  
Darren C. Henstridge ◽  
Brian G. Drew ◽  
Melissa F. Formosa ◽  
Alaina K. Natoli ◽  
David Cameron-Smith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Sodium Nitroprusside ◽  
Glucose Uptake ◽  
Muscle Cells ◽  
Skeletal Muscle Cells ◽  
Nitric Oxide Donor

Effects of Nitric Oxide Donor Antioxidants Containing the Phenol Vitamin E Substructure and a Furoxan Moiety on Ischemia/Reperfusion Injury

2011 ◽  
Vol 59 (03) ◽  
pp. 111-116
Author(s):  
Antonella Di Stilo ◽  
Konstantin Chegaev ◽  
Loretta Lazzarato ◽  
Roberta Fruttero ◽  
Alberto Gasco ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vitamin E ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor

Neutrophils as mediators of human skeletal muscle ischemia-reperfusion syndrome

1992 ◽  
Vol 23 (6) ◽  
pp. 627-634 ◽  
Author(s):  
Lucia Formigli ◽  
Lola Domenici Lombardo ◽  
Chiara Adembri ◽  
Sandra Brunelleschi ◽  
Enrico Ferrari ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Ischemia Reperfusion ◽  
Muscle Ischemia

The nitric oxide donor molsidomine prevents ischemia/reperfusion injury of the adult rat small intestine

2003 ◽  
Vol 19 (4) ◽  
pp. 305-308 ◽  
Author(s):  
Hayrettin Öztürk ◽  
Mustafa Aldemir ◽  
Ali İhsan Dokucu ◽  
Yusuf Yağmur ◽  
Nihal Kilinç ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Rat Small Intestine ◽  
Adult Rat

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach

1996 ◽  
Vol 271 (1) ◽  
pp. G27-G35
Author(s):  
J. G. Wood ◽  
Q. Zhang ◽  
Z. Y. Yan ◽  
L. Y. Cheung
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Question Mark ◽  
Endothelin 1 ◽  
Vasoconstrictor Response ◽  
Anesthetized Dogs ◽  
Spermine Nonoate

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate inverted question mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor inverted question mark attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

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