Browsing by Subject "Nitric Oxide"
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Item Formation Kinetics of Nitric Oxide of Biodiesel Relative to Petroleum Diesel under Comparable Oxygen Equivalence Ratio in a Homogeneous Reactor(2011-10-21) Rathore, Gurlovleen K.Interest in biodiesel has piqued with advent of stringent emissions regulations. Biodiesel is a viable substitute for petroleum diesel because biodiesel produces significantly lower particulate and soot emissions relative to petroleum diesel. Higher nitric oxide (NO) emissions for biodiesel, however, are of primary concern in biodiesel-fueled engines. Search for an in-cylinder technique to reduce NO emissions for biodiesel has motivated studies to gain an improved understanding of fundamental factors that drive increase in NO emissions with biodiesel. Potential factors include fuel-bound oxygen, fuel-bound nitrogen and post-flame gas temperature. The role of fuel-bound oxygen however is debated in the literature. The research objective of this study is to computationally determine if biodiesel and petroleum diesel yield equivalent concentrations of NO with the same oxygen equivalence ratio in a 0-D homogeneous reactor, to explain the role of fuel-bound oxygen in biodiesel on increases in NO emissions with biodiesel. The results from this study indicate that the biodiesel surrogate yields higher NO emissions than the n-heptane because of its lower oxygen consumption efficiency. The lower oxygen consumption efficiency for biodiesel is likely because of the slower decomposition of the individual components and the blending ratios of the biodiesel surrogate blend. The relative differences in combustion efficiency of individual components of the biodiesel blend suggest this conclusion. The more efficient burning of the methyl esters relative to the n-heptane in biodiesel surrogate perhaps indicates the favorable role of fuel-bound oxygen in the fuel?s combustion. The low utilization of oxygen by the biodiesel surrogate could not be explained in this study. The dominance of NO2 H ? NO OH and N NO ? N2 O mechanisms during biodiesel combustion however explain the high NO emissions for the biodiesel surrogate relative to the n-heptane. The biodiesel may yield lower NO emissions than the petroleum diesel if the blending ratios for the biodiesel are adjusted such that combustion efficiency of biodiesel and petroleum diesel is same or the NO2 H ? NO OH and N NO ? N2 O mechanisms are suppressed during biodiesel combustion.Item Regulation of Endothelial Phenotype in Rat Soleus Muscle Feed Arteries: Influence of Aging and Exercise Training(2012-02-14) Trott, Daniel WayneAging is associated impaired endothelial function in the skeletal muscle vasculature which contributes to decreased ability to increase muscle blow during exercise. This endothelial dysfunction is mediated, primarily, by impairments in the nitric oxide (NO) pathway in the skeletal muscle vasculature. The major purpose of this dissertation is to determine the mechanisms that mediate age-related endothelial dysfunction in rat soleus feed artery (SFA) and determine whether exercise training ameliorates this impairment in endothelial function. Therefore in these series of studies we sought to test three major hypotheses: 1) That exercise training reverses age-related decrements in endothelium-dependent dilation in SFA and that this improved endothelium-dependent dilation is the result of increased NO bioavailability due to increased content and phosphorylation of eNOS and/or increased antioxidant enzyme content; 2) That age-related endothelial dysfunction in rat SFA is mediated in part, by NAD(P)H oxidase-derived reactive oxygen species (ROS); 3) and, that impaired endothelium-dependent dilation in senescent SFA is due to an impaired potential for p-eNOSser1177. To test these hypotheses, SFA from young (4 month) and old (24 month) Fischer 344 rats were isolated for either determination of endothelium-dependent and ?independent dilations or biochemical analyses. Results from these investigations suggest that 1) exercise training reverses the detrimental effects of aging on endothelial function in skeletal muscle feed arteries by enhancing the capacity to scavenge superoxide, increasing the bioavailability of NO; 2) ROS contribute to impaired endothelium-dependent dilation in old SFA; whereas, ROS appear to play a role in ACh-mediated dilation in SFA from young rats; 3) and, that the PI3 kinase/protein kinase B (Akt)/eNOS pathway is preserved with age.Item Suppression of manganese-dependent production of nitric oxide in astrocytes: implications for therapeutic modulation of glial-derived inflammatory mediators(2009-05-15) Wright, Tyler T.Primary cultured astrocytes were treated with Mn in the absence and presence of proinflammatory cytokines to determine their effect upon stimulation of nitric oxide (NO) production. Treatments of manganese and cytokines raised NO production to intermediate levels, whereas combined treatment raised NO creation to much greater levels. Furthermore, this combined treatment differed from control only in its ability to elevate cellular NO levels at 24 hours, but not at earlier time points. Combined exposure in astrocytes derived from mice lacking the nos2 gene prevented any increase in production of NO. Thus, manganese and cytokines enhance NO production through activation of the nos2 gene. Additionally, pharmacologic ligands of the peroxisome proliferator-activated receptor gamma (PPAR?) were used to test the role of this orphan nuclear receptor in modulating Mn-dependent production of NO. The agonist, 1,1-Bis(3?-indolyl)-1-(p-trifluormethylphenyl) methane (cDIM1) diminished NO in a dose-dependent manner, whereas addition of the PPAR? antagonist, GW 9662, amplified cellular NO production, also in a dose-dependent fashion. Moreover, it was observed that NO production was both attenuated and augmented at similar rates, suggesting the agonist and antagonist work through similar mechanisms. To clarify the means by which NO levels are manipulated by PPAR?, we measured activation levels of the transcription factor NF-?B, a primary factor resulting in expression of NOS2. We found that NF-?B was slightly activated in cells treated solely with manganese or cytokines, whereas cells treated with both manganese and cytokines showed the highest levels of activation. Also, we found that these ligands function through an NF-?B dependent mechanism. Treatment of cDIM1 to astrocytes already treated with manganese and cytokines caused decreased activation of NF-?B, while addition of GW9662 to similarly treated cells resulted in increased activation of NF-?B. While these compounds were effective at manipulating induction of the nos2 gene, they had no effect on induction of guanosine tri-phosphate cyclohydrolase (GTPCH) the rate limiting enzyme for the production of tetrahydrobiopterin (BH4), a cofactor essential to the conversion of arginine to NO, Thus, these novel PPAR? ligands can influence manganese- and cytokine-induced production of NO by an NF-?B dependent mechanism.