Role of constitutive nitric oxide synthase and peroxynitrite production in a rat model of splanchnic artery occlusion shock
References (40)
- et al.
Eur J Pharmacol
(1992) - et al.
Arch Biochem Biophys
(1992) - et al.
FEBS Letters
(1995) - et al.
J Mol Cell Cardiol
(1995) - et al.
J Biol Chem
(1996) - et al.
Gastroenterology
(1995) - et al.
J Biol Chem
(1994) - et al.
J Biol Chem
(1996) Am J Physiol
(1993)- et al.
Am J Physiol
(1990)
Am J Physiol
Circ. Shock
New Engl J Med
FASEB
Current Top Microbiol Immunol
Cardiovasc Res
Cardiovasc Res
Br J Pharmacol
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A fresh frozen plasma to red blood cell transfusion ratio of 1:1 mitigates lung injury in a rat model of damage control resuscitation for hemorrhagic shock
2015, American Journal of Emergency MedicineEffect of Lactobacillus plantarum and l-arginine against endotoxin-induced liver injury in a rat model
2011, Life SciencesCitation Excerpt :Previous studies have shown that NO reduce mucosal injury after ischemia/reperfusion (Kubes and Granger, 1992) and decrease lung injury caused by intestinal ischemia (Terada et al., 1996). On the other hand, it has been documented that NO reacts with superoxide anion leading to the formation of peroxynitrite (ONOO) an oxidative agent capable of causing tissue damage (Cuzzocrea et al., 1998; Takada et al., 1998). For this reason, we investigated the role of NO in liver injury.
Protective effect of NAC preconditioning against ischemia-reperfusion injury in piglet small bowel transplantation: Effects on plasma TNF, IL-8, hyaluronic acid, and NO
2011, Journal of Surgical ResearchCitation Excerpt :Nitric oxide is a gaseous molecule produced by a family of P450-like enzymes termed NO synthases (NOS) that convert L-arginine and oxygen into L-citrulline and NO. There are two types of NO synthases (constitutive and inducible). As far as NO serum concentration after reperfusion is concerned, conflicting results have been reported thus far, partly explained by its origin (iNOS or cNOs) [28, 29]. Nitric oxide has been shown to have a protective effect, particularly in its constitutive form.
Effects of oral administration of L-arginine, L-NAME and allopurinol on intestinal ischemia/reperfusion injury in rats
2011, Life SciencesCitation Excerpt :We detected ONOO− footprint, NT, which was significantly increased during reperfusion in the Control group without relative increases in iNOS activity. Other researchers have also observed that NT and iNOS do not increase in parallel during I/R (Cuzzocrea et al., 1998); however, in the l-Arg group, the high levels of NT and iNOS were observed in parallel during the entire experimental period. Interestingly, serum nitrite was significantly increased in the l-NAME group after 8 and 24 h of reperfusion.
Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury-A Review
2008, Journal of Surgical ResearchCitation Excerpt :Kubes et al. [83] have demonstrated in the intestine that eNOS has a protective effect on intestinal mucosa, while increased iNOS has been shown to increase mucosal apoptosis by generation of free radicals such as peroxynitrate [105, 106]. However recent studies have shown that the production of peroxynitrate may be associated with loss of eNOS rather than increased iNOS production [107]. This observation suggests a dichotomous role for NO in IR injury with small quantities of NO produced by eNOS, reducing IRI, while excessive NO due to iNOS, causing deleterious effects.
Attenuation of contractile dysfunction by atorvastatin after intestinal ischemia reperfusion injury in rats
2007, European Journal of Pharmacology