As determined 4 h after ingestion by a tracer-based method using iv [(15)N(2)-(guanido)]-arginine, the whole-body NO production fell by 27 +/- 9% postprandially.

This is the first study evidencing that a meal challenge that impairs the stimulated, NO-mediated, vascular response also reduces whole-body basal NO production and bioavailability. Postprandial pathophysiology may build on this general, fundamental alteration in NO production. BIBF 1120 price (C) 2009 Elsevier Inc. All rights reserved.”
“A low reaction rate with nitric oxide (NO) is one of the important characteristics

of hemoglobin (Hb)-based oxygen carriers. The reaction rate between oxyHb and NO is usually measured by stopped-flow spectrophotometry. However, the reported rates vary due to the difficulty of accurately determining the NO concentration and the limit of the instrument dead time. To circumvent

these problems, we developed an experiment using oxymyoglobin (oxyMb) to compete selleck inhibitor with oxyHb for NO that is released from an NO donor. Determination of the rate constants in the competition experiment no longer depends on accurate measurement of time or NO concentration, since this approach instead measures the ratio of rate constants for the reaction of oxyHb and oxyMb with NO. For recombinant mutant Hb alpha(L29F)beta the rates for alpha(L29F) and beta are approximately 15- and 1.6-fold smaller than for wild-type Quisqualic acid Hb. In conclusion, the competition experiment provides

an alternative method for determination of relative reaction rates of recombinant Hb subunits with NO. (C) 2009 Elsevier Inc. All rights reserved.”
“Tissue ischemia and ischemia-reperfusion (I/R) remain sources of cell and tissue death. Inability to restore blood flow and limit reperfusion injury represents a challenge in surgical tissue repair and transplantation. Nitric oxide (NO) is a central regulator of blood flow, reperfusion signaling and angiogenesis. De novo NO synthesis requires oxygen and is limited in ischemic vascular territories. Nitrite (NO(2-)) has been discovered to convert to NO via heme-based reduction during hypoxia, providing a NO synthase independent and oxygen-independent NO source. Furthermore, blockade of the matrix protein thrombospondin-1 (TSP1) or its receptor CD47 has been shown to promote downstream NO signaling via soluble guanylate cyclase (sGC) and cGMP-dependant kinase. We hypothesized that nitrite would provide an ischemic NO source that could be potentiated by TSP1-CD47 blockade enhancing ischemic tissue survival, blood flow and angiogenesis. Both low dose nitrite and direct blockade of TSP1-CD47 interaction using antibodies or gene silencing increased acute blood flow and late tissue survival in ischemic full thickness flaps. Nitrite and TSPI blockade both enhanced in vitro and in vivo angiogenic responses.