Veterinary Research Communications, 29(Suppl. 2) (2005) 199–202 DOI: 10.1007/s11259-005-0042-0 C  Springer 2005 Nitrosylhemoglobin as a Potential Bioactive Storage form of Nitric Oxide (NO) F. Pirrone 1, ∗ , M. Albertini 1 , S. Mazzola 1 , G. Aldini 2 , M. Orioli 2 , M. Carini 2 , R. Maffei Facino 2 and M.G. Clement 1 1 Department of Animal Pathology, Hygiene and Public Veterinary Healt, Section of Biochemistry and Physiology, Faculty of Veterinary Medicine, University of Milan, 20133 Milan, Italy; 2 Chemical Pharmaceutical and Toxicological Institute, University of Milan, 20100 Milan, Italy ∗ Correspondence: E-mail: federica.pirrone@unimi.it Pirrone, F., Albertini, M., Mazzola, S., Aldini, G., Orioli, M., Carini, M., Maffei Facino, R. and Clement, M.G., 2005. Nitrosylhemoglobin as a potential bioactive storage form of nitric oxide (NO). Veterinary Research Communications, 29(Suppl. 2), 199–202 Keywords: nitric oxide, nitrosylhemoglobin, pig Abbreviations: CO, cardiac output; MAP, mean systemic arterial pressure; MPAP, mean pulmonary arterial pressure; NO, nitric oxide; SNP, sodium nitroprusside INTRODUCTION Nitric oxide is a critical regulator of endothelial functions and vascular smooth muscle tone. In addition, NO inhibits platelet aggregation and leukocyte adhesion, modulates respiration and exerts antioxidant and anti-inflammatory activity (Gladwin et al., 2000) . NO is syn- thesized from L-arginine by endothelial cell NO synthase. Since it has a very short half-life in the blood (approximately 2 ms), NO has been considered a simple paracrine mediator. An emerging theory, however, is that NO additionally functions through an endocrin mech- anism, with the formation of intravascular molecules able to stabilize NO bioactivity and deliver it at a distance from the site of generation (Gladwin et al., 2004). Among the proposed bioactive storage forms of NO, there is evidence of a pivotal role of nitrosylhemoglobin [HbFe(II)NO] and nitrites (NO − 2 ) Lane et al. (2002). Despite the unequivocal evidence of the formation of HbFe(II)NO, generated by an additional mechanism of NO to free heme, its ability to release NO is still not known. In fact, while the reduction of nitrites to NO in ischemic/hypoxic regions has been already described, hemodynamic effects induced by nitrosylhemoglobin must be elucidated. The aim of this work was therefore to shed light on the bioavailability of nitrosylhe- moglobin after i.v. infusion of a saturated NO solution, in an experimental physiological model. The hemodynamic properties of nitrosylhemoglobin were also studied and com- pared with the hemodynamic effects that followed the administration of an NO-donor, such as sodium nitroprusside (SNP). 199