Increased plasma levels of nitric oxide and malondialdehyde in dogs infected by Ehrlichia canis: Effect of doxycycline treatment

2021 ◽  
Author(s):  
A. Pedreañez ◽  
J. Mosquera-Sulbaran ◽  
N. Muñoz
Keyword(s):  
Nitric Oxide ◽  
Plasma Levels ◽  
Ehrlichia Canis ◽  
Doxycycline Treatment

The MTHFR 677 C/T polymorphism influences plasma levels of adhesion molecules and nitric oxide

2008 ◽  
Vol 121 (4) ◽  
pp. 549-554 ◽  
Author(s):  
Suh-Hang Hank Juo ◽  
Yi-Chu Liao ◽  
Chen-Ling Kuo ◽  
Yihsin Wang ◽  
Ching-Shan Huang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Adhesion Molecules ◽  
Plasma Levels

Induction of Vasoactive Substances Differs in LPS-Induced and TF-Induced DIC Models in Rats

2002 ◽  
Vol 88 (10) ◽  
pp. 663-667 ◽  
Author(s):  
Mariko Okudaira ◽  
Tomotaka Yoshida ◽  
Yasuo Ontachi ◽  
Masahide Yamazaki ◽  
Eriko Morishita ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Organ Dysfunction ◽  
Disseminated Intravascular Coagulation ◽  
Rat Model ◽  
Plasma Levels ◽  
Fibrinolytic Activity ◽  
Tail Vein ◽  
Vasoactive Substances ◽  
Rat Tail

SummaryWe have investigated the role of two vasoactive substances, nitric oxide (NO) and endothelin (ET), in the pathophysiology of disseminated intravascular coagulation (DIC), using two types of DIC models. Experimental DIC was induced by sustained infusion of 0.1, 1, 10, or 50 mg/kg lipopolysaccharide (LPS), or 3.75 U/kg thromboplastin (TF), for 4 h via the rat tail vein. Plasma levels of both NOX (metabolites of NO) and ET were significantly increased following infusion of 0.1 mg/kg or greater of LPS in the LPS-induced DIC rat model. In contrast, although a marked increase in the plasma levels of NOX was observed, only a slight increase in plasma ET levels was seen in the TF-induced DIC rat model. No significant differences in the plasma levels of platelets or thrombin-ATIII complex were observed among the TF-induced and LPS (50 mg/dl)-induced DIC models. However, plasma NOX levels rose significantly higher in the TF-induced model, relative to the LPS-induced model (p <0.01). Conversely, plasma ET levels were significantly greater after LPS-induction, compared to TF-induction, of DIC (p <0.01). Vasoconstriction, as well as depressed fibrinolytic activity, may be additional factors leading to severe organ dysfunction in the LPS-induced DIC rat model. Moreover, vasodilatation, as well as enhanced fibrinolytic activity, may help to prevent rats from severe organ dysfunction in the TF-induced DIC model. Our results suggest that modulator of vasoactive substances should be examined in the treatment of DIC.

scholarly journals Plasma levels of interleukin-10 and nitric oxide in response to two different desflurane anesthesia flow rates

2014 ◽  
Vol 64 (4) ◽  
pp. 292-298 ◽  
Author(s):  
Dilek Kalaycı ◽  
Bayazit Dikmen ◽  
Murat Kaçmaz ◽  
Vildan Taşpınar ◽  
Dilşen Örnek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Plasma Levels ◽  
Interleukin 10 ◽  
Flow Rates

Increased nitric oxide production in platelets from severe chronic renal failure patients

2011 ◽  
Vol 89 (2) ◽  
pp. 97-102 ◽  
Author(s):  
Mariana Alves de Sá Siqueira ◽  
Tatiana M.C. Brunini ◽  
Natália Rodrigues Pereira ◽  
Marcela Anjos Martins ◽  
Monique Bandeira Moss ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Platelet Aggregation ◽  
Plasma Levels ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
No Production ◽  
Dialysis Treatment ◽  
Cgmp Pathway

Nitric oxide (NO) production occurs through oxidation of the amino acid l-arginine by NO synthase (NOS). NO inhibits platelet activation by increasing the levels of cyclic guanosine monophosphate (cGMP), thus maintaining vascular homeostasis. Our group previously demonstrated ( da Silva et al. 2005 ) an enhancement of the l-arginine–NO–cGMP pathway in platelets taken from chronic renal failure (CRF) patients on haemodialysis associated with reduced platelet aggregation. We investigate the platelet l-arginine–NO–cGMP pathway, platelet function, and inflammation from patients in CRF on conservative treatment. A total of 42 CRF patients and 42 controls (creatinine clearance = 27 ± 3 vs. 93 ± 1 mL per min per 1.73 m2, respectively) participated in this study. NOS activity and expression and cGMP concentration were measured in platelets. Platelet aggregation induced by collagen or ADP was evaluated and plasma levels of fibrinogen were determined by the Clauss method. A marked increase in basal NOS activity was seen in undialysed CRF patients compared with controls, accompanied by an elevation of fibrinogen plasma levels. There were no differences in expression of NOS and in cGMP levels. In this context, platelet aggregation was not affected. We provide the first evidence of increased intraplatelet NO biosynthesis in undialysed CRF patients, which can be an early marker of future haemostatic abnormalities during dialysis treatment.

Recombinant Tissue Factor Pathway Inhibitor Prevents Lipopolysaccharide-induced Systemic Hypotension in Rats by Inhibiting Excessive Production of Nitric Oxide

2001 ◽  
Vol 86 (12) ◽  
pp. 1573-1577 ◽  
Author(s):  
Perenlei Enkhbaatar ◽  
Mitsuhiro Uchiba ◽  
Hirotaka Isobe ◽  
Hiroaki Okabe ◽  
Kenji Okajima
Keyword(s):  
Nitric Oxide ◽  
Tissue Factor ◽  
Plasma Levels ◽  
Tissue Factor Pathway Inhibitor ◽  
Factor Viia ◽  
Inos Mrna ◽  
Induced Hypotension ◽  
Inos Activity ◽  
Tnf Α ◽  
Tissue Factor Pathway

SummaryExcessive production of nitric oxide (NO) by the inducible form of NO synthase (iNOS) plays a key role in the development of endotoxin shock. Tumor necrosis factor-α (TNF-α) induces iNOS, thereby contributing to the development of shock. We recently reported that recombinant tissue factor pathway inhibitor (r-TFPI), an important inhibitor of the extrinsic pathway of the coagulation system, inhibits TNF-α production by monocytes. In this study, we investigated whether r-TFPI could ameliorate hypotension by inhibiting excessive production of NO in rats given lipopolysaccharide (LPS). Pretreatment of animals with r-TFPI prevented LPS-induced hypotension. Recombinant TFPI significantly inhibited the increases in both the plasma levels of NO2 -/NO3 - and lung iNOS activity 3 h after LPS administration. Expression of iNOS mRNA in the lung was also inhibited by intravenous administration of r-TFPI. However, neither DX-9065a, a selective inhibitor of factor Xa, nor an inactive derivative of factor VIIa (DEGR-F.VIIa) that selectively inhibits factor VIIa activity, had any effect on LPS-induced hypotension despite their potent anticoagulant effects. Moreover, neither the plasma levels of NO2 -/NO3 - nor lung iNOS activity were affected by administration of DX-9065a and DEGR-F.VIIa. These results suggested that r-TFPI ameliorates LPS-induced hypotension by reducing excessive production of NO in rats given LPS and this effect was not attributable to its anticoagulant effects, but to the inhibition of TNF-α production.

scholarly journals Asymmetric dimethylarginine, oxidative stress, and vascular nitric oxide synthase in essential hypertension

2009 ◽  
Vol 296 (2) ◽  
pp. R195-R200 ◽  
Author(s):  
Dan Wang ◽  
Svend Strandgaard ◽  
Jens Iversen ◽  
Christopher S. Wilcox
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Essential Hypertension ◽  
Nitric Oxide Synthase ◽  
Plasma Levels ◽  
Asymmetric Dimethylarginine ◽  
Lipid Peroxidation Product ◽  
Individual Values ◽  
Oxide Synthase

We reported impaired endothelium-derived relaxation factor/nitric oxide (EDRF/NO) responses and constitutive nitric oxide synthase (cNOS) activity in subcutaneous vessels dissected from patients with essential hypertension ( n = 9) compared with normal controls ( n = 10). We now test the hypothesis that the patients in this study have increased circulating levels of the cNOS inhibitor, asymmetric dimethylarginine (ADMA), or the lipid peroxidation product of linoleic acid, 13-hydroxyoctadecadienoic acid (HODE), which is a marker of reactive oxygen species. Patients had significantly ( P < 0.001) elevated (means ± SD) plasma levels of ADMA (PADMA, 766 ± 217 vs. 393 ± 57 nmol/l) and symmetric dimethylarginine (PSDMA: 644 ± 140 vs. 399 ± 70 nmol/l) but similar levels of l-arginine accompanied by significantly ( P < 0.015) increased rates of renal ADMA excretion (21 ± 9 vs. 14 ± 5 nmol/μmol creatinine) and decreased rates of renal ADMA clearance (18 ± 3 vs. 28 ± 5 ml/min). They had significantly increased plasma levels of HODE (PHODE: 309 ± 30 vs. 226 ± 24 nmol/l) and renal HODE excretion (433 ± 93 vs. 299 ± 67 nmol/μmol creatinine). For the combined group of normal and hypertensive subjects, the individual values for plasma levels of ADMA and HODE were both significantly ( P < 0.001) and inversely correlated with microvascular EDRF/NO and positively correlated with mean blood pressure. In conclusion, elevated levels of ADMA and oxidative stress in a group of hypertensive patients could contribute to the associated microvascular endothelial dysfunction and elevated blood pressure.

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