Role of nitric oxide synthase types II and III in early protection against endotoxin-induced lung injury (part 1)

endotoxin-induced lung injury (part 1)

Following administration of lipopolysaccharide (LPS) from Escherichia coli (2 mg/kg/min intravenously over 10 mins), Sprague-Dawley rats develop a two-phase hypotensive response (Figure 1). The immediate, transient phase of hypotension starts 2 to 3 mins after LPS administration begins, reaches its peak at 15 mins and is followed by the late phase that starts 70 to 90 mins after LPS administration and lasts several hours until the animal’s death.In the early 1990s, it was proposed that the second phase of arterial hypotension and vasoplegia evoked by LPS from E coli in laboratory animals might be mediated by endogenous nitric oxide produced from inducible nitric oxide synthase (NOS-II) by LPS . Some authorities in the field consider an initial fall in blood pressure that occurs some minutes after administration of LPS to be an epiphenomenon – its mechanisms not worthy of study. You will be sure to enjoy shopping at a pharmacy that offers best quality drugs any moment of the day you need them. So, without further ado, why not visit this *pharmacy and discover how low prices can be.

In a recent publication , we showed by using a direct continuous assay of nitric oxide that administering LPS to rats evokes an acute burst of nitric oxide generation in lung parenchyma, probably by constitutive NOS (NOS-III), mirrored by a concomitant drop in arterial blood pressure. Pretreatment of rats with a nonselective NOS inhibitor (NG-nitro-L-arginine [L-NNA]) abolished the LPS-induced rise of nitric oxide levels in the lung parenchyma, and then LPS killed the rats, among other symptoms of acute lung injury.


This entry was posted in Lung injury and tagged 1-Amino-2-hydroxy-guanidine, Endotoxic shock, NG-nitro-L-arginine, Nitric oxide, Nitric oxide synthase type II, Nitric oxide synthase type III, S-nitroso-N-acetyl-penicillamine.