Prevention by NCX 4016, a nitric oxide-donating aspirin, but not by aspirin, of the acute endothelial dysfunction induced by exercise in patients with intermittent claudication.

@article{Gresele2007PreventionBN,
  title={Prevention by NCX 4016, a nitric oxide-donating aspirin, but not by aspirin, of the acute endothelial dysfunction induced by exercise in patients with intermittent claudication.},
  author={Paolo Gresele and Rino Migliacci and A. Procacci and Paola De Monte and Erminio Bonizzoni},
  journal={Thrombosis and haemostasis},
  year={2007},
  volume={97 3},
  pages={
          444-50
        }
}
Ischemia/reperfusion damage evokes systemic inflammation and endothelial dysfunction in patients with intermittent claudication. We compared the effects of aspirin with those of a nitric oxide-donating aspirin in preventing the acute, systemic endothelial dysfunction provoked by exercise-induced ischemia of the lower limbs in patients with intermittent claudication. In a prospective, randomized, single-blind, parallel-groups trial among 44 patients with intermittent claudication we compared… 

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References

SHOWING 1-10 OF 47 REFERENCES

Nitric Oxide–Releasing Aspirin Derivative, NCX 4016, Promotes Reparative Angiogenesis and Prevents Apoptosis and Oxidative Stress in a Mouse Model of Peripheral Ischemia

Pretreatment with the new oral NO-releasing aspirin derivative stimulates reparative angiogenesis and prevents apoptosis and oxidative stress, thereby alleviating the consequences of supervening arterial occlusion.

Pharmacologic profile and therapeutic potential of NCX 4016, a nitric oxide-releasing aspirin, for cardiovascular disorders.

In phase II studies, NCX 4016 had favorable effects on effort-induced endothelial dysfunction in intermittent claudication and on platelet-activation parameters elicited by short-term hyperglycemia in type II diabetics, and in patients with type II diabetes the effects of NCX4016 on microalbuminuria and on some hemodynamic parameters were promising.

L-arginine protects from ischemia-reperfusion-induced endothelial dysfunction in humans in vivo.

It is demonstrated that the NO substrate l-arginine significantly attenuates ischemia-reperfusion-induced endothelial dysfunction in humans in vivo, suggesting that l- arginine may be useful as a therapeutic agent in the treatment of ischemIA-rePerfusion injury in humans.

Exercise training reduces the acute inflammatory response associated with claudication.

This study for the first time demonstrates that the exercise training of claudicants is beneficial, not only in terms of improving their walking distance, but also by decreasing the injurious effects of IRI that occur during claudication.

Gastrointestinal safety of NO-aspirin (NCX-4016) in healthy human volunteers: a proof of concept endoscopic study.

The concept that addition of an NO-donating moiety to aspirin results in a new chemical entity that maintains cyclooxygenase-1 and platelet inhibitory activity while nearly avoiding gastrointestinal damage is proven.

Acute Systemic Inflammation Impairs Endothelium-Dependent Dilatation in Humans

S typhi vaccine generates a mild inflammatory reaction associated with temporary but profound dysfunction of the arterial endothelium in both resistance and conduit vessels to both physical and pharmacological dilator stimuli, which might explain the association between infection and inflammation and the enhanced risk of an acute cardiovascular event.

Functional and Biochemical Analysis of Endothelial (Dys)function and NO/cGMP Signaling in Human Blood Vessels With and Without Nitroglycerin Pretreatment

It is concluded that long-term NTG treatment induces endothelial dysfunction and impaired vascular NO/cGMP signaling in humans, which can be monitored by measuring P-VASP levels.

Nonsteroidal Antiinflammatory Drugs Aggravate Acute Myocardial Ischemia in the Perfused Rabbit Heart: A Role for Prostacyclin

The present data suggests that the deleterious effect of nonsteroidal antiinflammatory drugs in low flow myocardial ischemia and reperfusion damage may be associated with removal of PGI2 and PGE2 from ischemic myocardium.