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Objectives. To assess the possibility to prevent the disturbances of nitric oxide (NO) formation and action system in prenatally stressed rats with the help of fish oil administered to their mothers during pregnancy against the background of stress. Material and methods. Outbred pregnant rats weighing 180-220 g were divided into equal groups (n=10): «Pregnant control», «Pregnant stress», «Pregnant control + fish oil», «Pregnant stress+fish oil». Stress was reproduced by exposure to stressors on different days of pregnancy: food deprivation during one day, contact with cats’ feces during one day, and immobilization in water (20 minutes, t°=23±2). Rats of the groups «Pregnant control + fish oil» and «Pregnant stress + fish oil» received 0.1 ml of fish oil (Biosola, Lithuania) as a gavage at a daily dose of 60 mg/kg of eicosapentaenoic and docosahexaenoic acids; rats of groups «Pregnant control» and «Pregnant stress» received an equivalent volume of starch solution (0.1 ml). In 3-month-old offspring (n=181), systolic, diastolic, and mean arterial pressure (SBP, DBP, MAP, respectively) were measured noninvasively; the concentration of endothelial and inducible isoforms of NO-synthase (eNOS and iNOS, respectively), cyclic guanosine monophosphate (cGMP), asymmetric dimethylarginine (ADMA) was determined in blood serum by ELISA; the content of nitrates/nitrites (NO3-/NO2-), diene conjugates (DC), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase was determined spectrophotometrically in blood serum. Results. Fish oil which was administered to pregnant rats under stress led to the increase of reduced compared with control males content of eNOS, cGMP, SOD, catalase, NO3-/NO2- (by 10.7%, 48.3%, 62.6%, 31.3%, 91.7%, respectively); the decrease of increased concentration of iNOS, ADMA, DC, MDA (by 21.8%, 37.4%, 61.2%, 75.9%, respectively) in the blood serum of male offspring. In female offspring of group «Pregnant stress + fish oil» the decrease of increased content of iNOS, DC, MDA (by 25.8%, 2.6 and 4.9 times, respectively) with the increase of reduced concentration of NO3-/NO2-, SOD (by 84.6%, 52%, respectively) were determined in the blood serum. The introduction of fish oil to pregnant rats against the background of stress prevented SBP, DBP, and MAP increasing in the offspring. Conclusions. The administration of fish oil to rats during pregnancy under chronic stress prevents the impairment of NO production and action in the offspring.

This study provides new quantitative NO concentrations measurements in n-propanol + air and i-propanol + air flames together with a new combustion kinetic model. The heat flux method was employed to stabilize propyl alcohols flames and the initial gas conditions were set to 323 K, 1 atm, and Φ=0.7–1.4. Saturated laser-induced fluorescence was employed to measure NO concentration in the post-combustion region. The presented and literature models, namely the POLIMI and Bohon et al. (2018) kinetic mechanisms, were assessed against new experimental data. Experimental results showed a higher NO formation in the thermal zone for n-propanol flames, whereas i-propanol flames indicate a higher amount of NO formed at fuel-rich conditions. Overall among the tested models, the present mechanism exhibited the best agreement in emulating NO experimental profiles; conversely, numerical simulations from the POLIMI model showed significant inconsistencies at fuel-rich conditions and the Bohon et al. (2018) model was unable to reproduce the measured data, notably underpredicting experimental values at all investigated conditions. However, the present model manifested some uncertainties in reproducing NO formation in the prompt region; therefore, in connection with this important aspect, the new experimental data obtained in this work will provide a valid support to further develop more reliable kinetic models.

Recent years have seen an increase in interest in the identification of additional genetic factors for cerebral stroke. A large number of studies have been run with the aim of verifying genetic influences on the risk of developing both ischemic and hemorrhagic stroke. This article discusses the main genes for susceptibility and genetic polymorphisms associated with the development of this disease. An important role in the occurrence of stroke is played by genetic factors controlling the processes of inflammation, blood clotting, lipid metabolism, nitric oxide formation, the functioning of the renin–angiotensin–aldosterone system, and homeostasis. Complex analysis of a number of genes allows patients with the greatest predisposition to developing the disease to be identified with the aims of providing state-of-the-art prophylaxis and reducing the burden of stroke.

Background: Nitric oxide (NO) is a gaseous substance, which act as a key factor on the regulation of some physiological systems activity (e.g. cardiovascular, skeletal), since decrease on NO biodisponibility, such as on the pathway responsible for its production, lead to impairment on body homeostasis. Besides chronic pathological conditions, senescence — which is conceited as the healthy aging — NO levels and its pathway also can be found decreased. In front of this scenario, it is possible observe that there is necessity of therapies that act collaborating with the maintaining of a favorable environment to NO synthesis, as well to development of its functions during aging. Some trial has been observed in animals and in human beings the capacity of physical exercise to act collaborating to NO activity maintaining during senescence and senility. Objectives: To evaluate the effect of physical training on activity of pathway responsible for NO formation, as well as its blood concentrations in animal and elderly human models. Methods: A literature search was performed in the PubMed, Web of Science, Scielo and Lilacs databases, that evaluated the effects of physical training and nitric oxide formation in animal and elderly human models. Results: According to the studies reviewed in this research, pathway of the NO synthesis improves through physical exercise in animal and elderly human models. Conclusion: Scientific evidences demonstrate effectiveness of the physical exercise in inhibiting decrease of bioavailability in NO which accompanies senescence, greater magnitude and senility.

Thermal nitric-oxide (NOx) formation in industrial furnaces due to local overheating is a widely known problem. Various industries made significant investments to reduce thermal NOx by varying the operating conditions and designs of the furnace. It is difficult to find the optimal operating conditions that minimize NOx formation in the furnace by trial and error methods. The high temperature in the furnace complicates performing experiments in the furnace. Numerical modeling can provide significant information in such cases. Therefore, the objective of this paper is to obtain a numerical model of the furnace in such a way that the operating conditions can be varied and examined. In this paper, a three-dimensional steady-state finite element model for the anode baking industrial furnace is discussed. The COMSOL Multiphysics software is used for modeling the non-premixed turbulent combustion and the conjugate heat transfer to the insulation lining. The cfMesh software is used for obtaining the mesh. The results show that the simulated temperature agrees well with the measured data from our industrial partner in regions distant from the flames. The analysis shows that by decreasing the fuel mass flow rate and increasing the fuel pipe diameter by 45%, the peak in thermal NOx ppm generated in the furnace decreases by 42%. The model is limited by the use of a single-step chemistry mechanism with an eddy dissipation combustion model and a simplified approach for radiation, such as the P1 approximation model. The model can be further improved by considering a detailed chemistry mechanism model for combustion and a discrete ordinate model for radiation.

The capacity of skimmed milk to neutralise increased reactive oxygen species (ROS) and to attenuate nitric oxide (NO) production, as well as to present cytoprotective effect at the intestinal level was assessed after in vitro gastro-intestinal digestion. The impact on ROS modulation was evaluated at a non-cytotoxic concentration of hydrogen peroxide (H2O2) in a co-culture of Caco-2 and HT-29 intestinal cells. In parallel, a cytotoxic concentration of H2O2 was used to study the effect of digested milk against induced cell apoptosis. Concerning induced NO production, it was evaluated using the model lipopolysaccharide (LPS)-stimulated RAW264.7 macrophage cells. Results showed that digested milk prevented the increase of basal ROS level in the intestinal epithelium and attenuated NO production by LPS-stimulated macrophage cells. In the H2O2-induced cytotoxicity assay, digested milk had no protection against apoptosis, confirmed by the failure in attenuating activated caspase-3/7.

Increasingly stringent regulations are imposed on nitric oxide (NO) due to its numerous, direct and indirect, deleterious effects on human health and the environment. A better control of the post-flame temperature field to contain the thermal (Zel’dovich) route resulted in significant reductions of engine emissions. An improved knowledge of the chemistry and rate of the secondary prompt, NNH, and N2O pathways is now required to decrease nitric oxide emissions further. For this effort, NO laser-induced fluorescence (LIF) measurements are presented for lean ( ϕ = 0.7 ), jet-wall, stagnation, premixed flames at pressures of 2, 4, and 8 atm. For all cases, the NO-LIF signal increases rapidly through the flame front, and relatively slowly in the post-flame region where the temperature is too low to sustain the thermal pathway. Nitric oxide mole fractions are inferred from the measurements and show that the pressure has a very weak, monotonic, adverse effect on NO formation. Reaction pathway analyses are applied to flame simulations performed with a thermochemical model capturing the general trends of the data to assess the contribution of each NO formation route. For all cases, the N2O pathway, which proceeds mostly in the flame front region, dominates. This route produces slightly larger amounts of NO at higher pressures, but the variation appears very limited when considering the termolecular nature of its initiation reaction. The thermal route is predicted to progress slowly in the post-flame region, which causes a shallow increase in the NO mole fraction. The NNH and prompt pathways generate small amounts of NO, and their contributions reduce with the pressure. Overall, the thermochemical model predicts that the formation of NO is relatively unaffected by the pressure, which is consistent with the experiments. The experimental dataset reported in this work is made available for the development of thermochemical models.

A vibration-specific approach is employed to describe vibrational relaxation and reactive processes in shock-heated air. Models are implemented that include results from recent theoretical calculat...

Modern data on biochemical patterns of nitric oxide biosynthesis in mammal cells from L-arginine in normoxic conditions is described. The attention of the authors is given to the results of the recent years on the structure and regulation features isoforms of NO-synthase. The emphasis is put on the latest conception of the compartmentalization of certain isoforms of these enzymes in cells and on the possibility of the directed transport of nitric oxide in the vascular wall. The central place in the review is devoted to issues on the endogenous formation of NO in mitochondria and its potential physiological significance. Our own results on the identification of NO in mitochondria of the uterine smooth muscle, biochemical characteristics of this process and NO possible role in Са2+ transport regulation by organelles are presented and discussed.

Made available in DSpace on 2020-12-12T02:23:29Z (GMT). No. of bitstreams: 0 Previous issue date: 2019-10-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) NAMPT is a biomarker for endothelial dysfunction, but its relationship with nitrite (marker of NO formation) and soluble fms-like tyrosine kinase-1 (sFLT-1) has not been previously evaluated in preeclampsia. Therefore, we measured plasma NAMPT and sFLT-1 levels using enzyme immunoassays and plasma nitrite concentrations using an ozone-based chemiluminescence assay. NAMPT was positively correlated to nitrite (r = 0.217; P = 0.034) and inversely related to sFLT-1 (r = −0.340; P = 0.029) in healthy pregnant women, but inversely related to nitrite (r = −0.259; P = 0.035) and positively correlated to sFLT-1 (r = 0.326; P = 0.007) in preeclamptic patients, suggesting that NAMPT inhibits NO formation and interacts with the antiangiogenic factor sFLT-1 in preeclampsia. Graduate Program in Genetics Institute of Biological Sciences Federal University of Minas Gerais (UFMG) Department of Pharmacology Institute of Biosciences Universidade Estadual Paulista (UNESP) Department of Physiology and Biophysics University of Mississippi Medical Center Department of Pharmacology Ribeirao Preto Medical School University of Sao Paulo Department of Gynecology and Obstetrics Ribeirao Preto Medical School University of Sao Paulo Department of Genetics Ecology and Evolution Institute of Biological Sciences Federal University of Minas Gerais (UFMG) Department of Pharmacology Institute of Biosciences Universidade Estadual Paulista (UNESP)

Background: Reperfusion or reopening of occluded vessels is the gold standard to terminate ischemia. However, early functional recovery after reperfusion is often low requiring inotropic intervention. Although catecholamines increase inotropy and chronotropy, they are not the best choice because they increase myocardial oxygen and substrate demand. As nitric oxide (NO) contributes to cardiac function, we tested the hypothesis that addition of citrulline during the onset of reperfusion improves post-ischemic recovery because citrulline can reenter arginine consumption of NO synthases (NOS) but not of arginases. Methods: Hearts from adult rats were used in this study, exposed to 45-minute global ischemia and subsequently reperfused for 180 minutes. Citrulline (100 µM) or arginine (100 µM) was added with reperfusion and remained in the perfusion buffer for 180 minutes. Nω-nitro-l-arginine methyl ester (l-NAME) was used to antagonize NOS activity. Results: Citrulline increased load-free cell shortening of isolated adult rat cardiomyocytes and improved left ventricular developed pressure (LVDP) under normoxic conditions, indicating that citrulline can affect heart function. Ischemia/reperfusion caused a constitutive loss of function during 3 hours of reperfusion, whereas citrulline, but not arginine, improved the functional recovery during reperfusion. This effect was attenuated by co-administration of l-NAME. Although citrulline increased the formation of nitrite, l-NAME attenuated this effect indicating again a positive effect of citrulline on NO formation. Citrulline, but not arginine, increased the expression of arginase-1 (protein and mRNA) but l-NAME attenuated this effect again. Collectively, citrulline improved the post-ischemic recovery in an NO-dependent way. Conclusions: Citrulline, known to block arginase and to support NO formation, improves the early functional recovery of post-ischemic hearts and may be an alternative to catecholamines to improve early post-ischemic recovery.

Amac: Bu calismada konvansiyonel veya endoskopik safen ven greft (SVG) cikarma tekniklerinin endotel butunlugune, inflamasyona ve nitrik oksit (NO) sentezi uzerine etkileri arastirildi. Ca­lis­ma­ pla­ni:­ Koroner arter baypas greft (KABG) cerrahisi sirasinda endoskopik (grup 1) ya da konvansiyonel (grup 2) teknikle 20 hastanin (23 erkek, 17 kadin; ort. yas 65.6±6.3 yil; dagilim 43-78 yil) 20 SVG segmenti alindi. Safen ven ornekleri oda sicakliginda bir saat sure ile heparinize kan icerisinde muhafaza edildi. Endotel fonksiyonunun belirleyicisi olarak, endoskopik ve konvansiyonel tekniklerle cikartilan SVG’lerdeki nitrik oksit (nitrat-NO3 ve nitrit-NO2) duzeyleri Greiss yontemiyle olculdu. Safen ven greft endotelinde olusan notrofil infiltrasyonun duzeyinin bir gostergesi olarak, safen doku myeloperoksidaz (MPO) aktivitesi de her iki grup icin olculdu. Bu olcum notrofilin neden oldugu safen ven endotel hasarini ve inflamasyon duzeyi belirlemede kullanildi. Bul gu lar: Nitrik oksit olusumu, NO3 ve NO2 olarak, (grup 1=34.18±5.43 mM, grup 2=25.73±2.52 mM, p

The reduction of trans- [Ru(NO)(NH 3 ) 4 (P(OEt) 3 )] 3+ ion was investigated in aqueous medium. Due to the phosphite ligand trans -effect and trans -influence, this complex selectively releases NO or HNO after one or two electrons reduction centered at the nitrosonium ligand (NO + ). These reactions were carried out through electrochemical reduction and using Eu 2+ and zinc amalgam, and the products were identified using electrochemical and spectroscopic techniques. Only the reduction of the nitrosonium ligand to nitric oxide is observed when europium is used as reductant. When the reaction is carried out with Zn(Hg), nitric oxide formation was not observed and N 2 O, an indirect marker of HNO, is detected in solution.

Allium hookeri, a member of the onion family, has long been mainly cultivated for food and medicinal use in Southeast Asia countries owing to its various biological properties. However, no studies of the anti-inflammatory effects of A. hookeri extracts have been conducted to date. Therefore, this study was investigated the potential of the methanol extract of A. hookeri to suppress the inflammation in lipopolysaccharide (LPS)-induced mouse macrophage RAW264.7 cells. This study was performed on macrophage cells that were pretreated with 0～500 μg/mL of methanol extract of A. hookeri root prior to LPS treatment. Treatment with methanol extract of A. hookeri root significantly inhibited LPS-induced nitric oxide formation in dose-dependent manner. Treatment of A. hookeri root also significantly decreased LPS-induced TNF-α and IL-6 production. The results of this study provide new evidence of the anti-inflammatory properties of A. hookeri and indicate that it may have a potential therapeutic use for the prevention and treatment of macrophage derived chronic immune diseases.

Nitric oxide (NO) is a key modulator of vascular homeostasis controlling critical functions related to blood flow, respiration, cell death and proliferation, and protecting the vasculature from pro-inflammatory and coagulative stresses. Inhibition of NO formation, and/or diversion of NO away from its physiological signalling targets lead to dysregulated NO bioavailability, a hallmark of numerous vascular and pulmonary diseases. Current concepts suggest that the balance between NO formation and NO scavenging is critical in disease development, with the corollary being that redressing the balance offers a target for therapeutic intervention. Evidence presented over the last two decades has seen red blood cells (RBCs) and haemoglobin specifically emerge as prominent effectors in this paradigm. In this symposium review article, we discuss recent insights into the mechanisms by which RBCs may modulate the balance between NO-formation and inhibition. We discuss how these mechanisms may become dysfunctional to cause disease, highlight key questions that remain, and discuss the potential impact of these insights on therapeutic opportunities.

Microscopic lymphatics produce nitric oxide (NO) during contraction as flow shear activates the endothelial cells. The valve leaflets and bulbous valve housing contain a large amount of endothelial nitric oxide synthase (eNOS) due both to many endothelial cells and increased expression of eNOS. Direct NO measurements indicate the valve area has a 30–50% higher NO concentration ([NO]) than tubular regions although both regions generate equivalent relative increases in [NO] with each contraction. We hypothesize that 1) the greater eNOS and [NO] of the bulb region would have greater effects to lower pumping activity of the overall lymphatic than occurs in tubular regions and 2), the elevated [NO] in the bulb region may be because of high NO production in the valve leaflets that diffuses to the wall of the bulb. Measurement of [NO] with a micropipette inside the lymphatic bulb revealed the valve leaflets generate ∼50% larger [NO] than the bulb wall in the in vivo rat mesenteric lymphatics. The valves add NO to the lymph that quickly diffuses to the bulb wall. Bradykinin locally released iontophoretically from a micropipette on both bulbs and tubes increased the [NO] in a dose-dependent manner up to ∼50%, demonstrating agonist activation of the NO pathway. However, pumping output determined by contraction frequency and stroke volume decreased much more for the bulb than tubular areas in response to the bradykinin. In effect, NO generation by the bulb area and its valves limits the pumped flow of the total lymphatic by lowering frequency and stroke volume of individual contractions.

Taking into account the data on oxidative transformation of hydroxamic acids to form nitric oxide and the similarity of their structure to the hydroxyarginine group being involved in the NO synthesis, we performed the study of biotransformation of salicylhydroxamic acid and N(4)-hydroxyasparagine in the liver tissues. According to the data from ESR spectroscopy, the compounds under study are inefficient NO donors in a biological system and their biological activities are mainly defined by the ability to chelate metal ions.

Numerical analysis has been carried out to investigate the combustion and NO formation and distribution characteristics using a beta probability density function (PDF) method in a three-dimensional...

In this paper an approach is presented, to calculate the nitric oxide exhaust of the diesel combustion. To be able to use the model in HIL-simulations, it must be executed in real-time on special hardware. Therefore the model was developed as an enhancement for a zero-dimensional model of the diesel combustion, which is already used for a HIL-test-bench. After a description of the diesel combustion-model, the calculation of the nitric oxide formation is presented, which is divided into three parts. First, the temperature of the hot combustion zone must be calculated, because the average in-cylinder temperature of the zero-dimensional model is not adequate as input data for the subsequent parts. With the temperature of the hot combustion zone, the equilibrium of the combustion products can be solved. The concentration of these species are finally used for the calculation of the nitric oxide formation by the well-known Zeldovich-mechanism.

In addition to the generation from specific nitric-oxide (NO) synthases, NO formation from nitrite occurs in ischemic tissues, such as the heart. Although NO binding to heme-centers is the basis for NO-mediated signaling as occurs through guanylate cyclase, it is not known if this process is triggered with physiologically relevant periods of sublethal ischemia and if nitrite serves as a critical substrate. Therefore electron paramagnetic resonance studies were performed to measure nitrosylheme formation during the time course of myocardial ischemia and reperfusion and the role of nitrite in this process. Rat hearts were either partially nitrite-depleted by nitrite-free buffer perfusion or nitrite-enriched by preinfusion with 50 μm nitrite. Ischemic hearts loaded with nitrite showed prominent spectra of six-coordinate nitrosyl-heme complexes, primarily NO-myoglobin, that increased as a function of ischemic duration, whereas in nonischemic-controls these signals were not seen. Total nitrosyl-heme concentrations within the heart were 6.6 ± 0.7 μm after 30 min of ischemia. Nitrite-depleted hearts also gave rise to NO-heme signals during ischemia, but levels were 8-fold lower. Nitrite-mediated NO-heme complex formation during ischemia was associated with activation of guanylate cyclase. Upon reperfusion, the levels of NO-heme complexes decreased 3-fold by the first 15 min but remained elevated for over 45 min. The decrease in NO-heme complex levels was paralleled by the formation of nitrate, suggesting the oxidation of heme-bound NO upon reperfusion. Thus, nitrite-mediated NO-heme formation occurs progressively during ischemia, with these complexes serving as a store of NO with concordant activation of NO signaling pathways.

We have established a technique to estimate the total rate of nitric oxide (NO) formation in mice, based on inhalation of a stable oxygen isotope (18O(2)). Changes of NO production with age were also studied.The experiments were performed in eight-week- (n=6) and eight-month-old (n=6-7), respectively, female (C57/Bl6xCBAca) mice. Pairs of conscious mice were kept in an air-tight closed system allowing breathing of a mixture containing 18O(2). The 18O(2)-technique was validated by L-NAME (10mg/kg) and lipopolysaccharide (LPS, 8 mg/kg) administration. The concentrations of O(2) and CO(2) in the system were controlled and plasma nitrate analyzed by GC/MS technique.NO formation was similar in young and old mice (young=7.68+/-1.47 vs. old = 6.25+/-1.49 micromol/kg/h, n.s.). Total NO production was reduced after L-NAME treatment in young animals by 91% and in old animals by 71% (p0.05 for both), whereas LPS administration increased NO production (114+/-17%, p0.05).Conclusion. NO formation is unaltered with age in mice. The 18O(2)-technique is a valid and specific technique to estimate whole body NO production in conscious mice.

Inflammation is a process consisting of a complex of cytological and chemical reactions which occur in and around affected blood vessels and adjacent tissues in response to an injury caused by a physical, chemical or biological insult. Much work has been performed in the past several years investigating inducible nitric oxide synthase (NOS, EC 1.14.13.39) and nitric oxide in inflammation. This has resulted in a rapid increase in knowledge about iNOS and nitric oxide. Nitric oxide formation from inducible NOS is regulated by numerous inflammatory mediators, often with contradictory effects, depending upon the type and duration of the inflammatory insult. Equine medicine appears to have benefited the most from the increased interest in this small, inflammatory mediator. Most of the information on nitric oxide in traditional veterinary species has been produced using models or naturally occurring inflammatory diseases of this species.

Background: Remote ischemic preconditioning (RIPC) induced by brief episodes of ischemia of the limb protects against organ damage by ischemia-reperfusion. It has been reported that RIPC improves endothelial function of the forearm in normal subjects and patients with coronary artery disease. However, the digital vascular endothelial response to RIPC has not been determined in healthy volunteers. Methods: This study was performed to examine effect of RIPC on fingertip digital vascular endothelial function by using endothelial pulse amplitude tonometry (EndoPAT) device and alteration in circulating nitric oxide(NO) level in peripheral blood. Ten healthy adult subjects (5 men, 5 women, mean age 25.2 years) had 3 cycles of 5 min ischemia alternating with 5 min reperfusion of the forearm. Another 10 healthy volunteers (6 men, 4 women, mean age 26.2 years) were used as the control group of sham and the cuff was inflated for 3 times at 10 mmHg for 5 minutes with 5-minute intervals. Fingertip digital vascular endothelial function of the ipsilateral arm was measured prior to first ischemia, 3h and 6h after the last episode of ischemia. Blood samples were taken from the contralateral arm prior to first ischemia, 3h and 6h after the last episode of ischemia. Results: Fingertip digital vascular endothelial function was significantly increase in 3h and 6h after the last RIPC intervention compared with the baseline condition(p Conclusion: The present findings demonstrate for the first time that transient RIPC contributes to improvement of digital vascular endothelial function and increase in circulating NO production in healthy volunteers. Our data provide a novel evidence to support that RIPC might gain even wider application not only in disease but also in health.

Objective: The purpose of this study was to investigate the role of nitric oxide (NO) during the development of fever and other symptoms of sickness behavior (i.e. anorexia, cachexia) in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. Methods: To determine the role of NO in turpentine-induced fever, we injected the NO synthase (NOS) inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) intraperitoneally simultaneously or 5 h after turpentine injection. Results: Rats responded with fever to intramuscular injection of 20 µl of turpentine that commenced 6 h after injection and reached peak values 11 h after injection. Although turpentine did not significantly alter food and water intake, it caused a drop in body weight. Rats injected with turpentine and treated with L-NAME responded with a substantial rise in fever, independently of the time of L-NAME injection. The rise in body temperature (Tb) due to turpentine injection began slightly sooner and reached the maximal Tb value faster in rats treated with L-NAME than in the ones treated with saline (control for L-NAME). The enhanced decrease in food and water intake in rats treated with a combination of L-NAME and turpentine was also observed. As a result, L-NAME-injected rats responded with a profound drop in body mass due to turpentine, independently of the time of L-NAME injection. L-NAME alone did not affect food and water intake, but slightly suppressed the gain of body mass. Conclusion: These results indirectly indicate that NO is involved in pyrogenic and behavioral responses in rats during turpentine abscess.

The GRIMECH version 2.11 chemical kinetics mechanism is modified to provide improved predictions of NO concentrations in high-pressure (1 < P < 15), low-temperature (1600 K–1850 K), premixed, flat, laminar, C2H6/O2/N2 flames. The modifications include adding 38 reactions to expand the C2 submechanism and using different reaction rate coefficients for the CH + N2 ↔ HCN + N reaction. The unmodified GRIMECH mechanism significantly underpredicts the NO concentrations in rich flames. In addition, the predictions from the original mechanism are poor qualitatively, particularly at the lower pressures studied. As the prompt-NO mechanism has been shown to be significant in the rich flames in this study, it is expected that the predictive errors of the unmodified mechanism are a result of deficiencies in the modeling surrounding the prompt-NO formation pathway. To account for the underprediction of prompt-NO, a different set of proposed reaction rate coefficients for the CH + N2 ↔ HCN + N are used in the revised model. The expansion of the C2 submechanism reactions enhances the existing C2 chemistry in the original mechanism, which was designed primarily for methane combustion. The modified mechanism provides good agreement with published NO concentration data from the postflame regions of flames from 1 to 9.16 atm. The revised mechanism does continue to underpredict the NO concentrations in 14.6-atm flames, although the predictions are improved qualitatively from the original mechanism at that pressure.