Role of Nitrite, a Nitric Oxide Derivative, in K-Cl Cotransport Activation of Low-Potassium Sheep Red Blood Cells

1998 ◽  
Vol 166 (3) ◽  
pp. 157-167 ◽  
Author(s):  
N.C. Adragna ◽  
P.K. Lauf
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Sheep Red Blood Cells ◽  
Low Potassium ◽  
Oxide Derivative

Protective role of caffeic acid phenethyl ester and erdosteine on activities of purine-catabolizing enzymes and level of nitric oxide in red blood cells of isoniazid-administered rats*

2008 ◽  
Vol 24 (8) ◽  
pp. 519-524 ◽  
Author(s):  
HR Yilmaz ◽  
E Uz ◽  
O Gökalp ◽  
N Özçelik ◽  
E Çiçek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Caffeic Acid ◽  
Blood Cells ◽  
Tap Water ◽  
Treated Group ◽  
Caffeic Acid Phenethyl Ester ◽  
Male Rats ◽  
Control Group

The aim of this experimental study was to investigate the possible role of nitric oxide (NO) and the activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the pathogenesis of isoniazid (INH)-induced oxidative damage in red blood cells (RBCs), and also to show the effect of caffeic acid phenethyl ester (CAPE) and erdosteine, antioxidants, in decreasing this toxicity. A total of 25 adult male rats were divided into four experimental groups as follows: control group ( n = 7), INH-treated group ( n = 6), INH + CAPE–treated group ( n = 6), and INH + erdosteine–treated group ( n = 6). INH, INH-CAPE, and INH-erdosteine–treated groups were treated orally with INH 50 mg/kg daily and with the tap water for 15 days. Control group was given only tap water. CAPE was intraperitoneally injected for 15 days at a dose of 10 μmol/kg. Erdosteine was treated orally for 15 days at a dose of 10 mg/kg/day. The injection of INH led to a significant increase in the activities of ADA, XO, and NO levels in RBCs of rats. Co-treatment with CAPE caused a significant decrease in the activities of ADA and XO and the levels of NO in RBCs. In addition, co-treatment with erdosteine caused a significant decrease in the activities of ADA and XO and the levels of NO in RBCs. The results of this study showed that ADA, XO, and NO may play an important role in the pathogenesis of INH-induced oxidative stress in RBCs. CAPE and erdosteine may have protective potential in this process and they may become a promising drug in the prevention of this undesired side effect of INH.

Effect of L-NAME on pressure-flow relationships in isolated rabbit lungs: role of red blood cells

1995 ◽  
Vol 269 (6) ◽  
pp. H1941-H1948 ◽  
Author(s):  
R. S. Sprague ◽  
A. H. Stephenson ◽  
R. A. Dimmitt ◽  
N. L. Weintraub ◽  
C. A. Branch ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Salt Solution ◽  
Blood Cells ◽  
Pulmonary Arteries ◽  
Physiological Salt Solution ◽  
Rabbit Lung ◽  
Pressure Flow ◽  
Arteries And Veins

Nitric oxide (NO) is produced by and relaxes pulmonary arteries and veins; however, a role for NO as a participant in the control of pulmonary vascular resistance (PVR) remains to be defined. Here we investigated the hypothesis that for NO to serve as a determinant of PVR in the rabbit requires the presence of blood. In isolated blood-perfused rabbit lungs, NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) increased PVR and the slope of the pressure-flow relationship. These effects of L-NAME were prevented by pretreatment with L-arginine. In contrast, in lungs perfused with a physiological salt solution, L-NAME had no effect on PVR or the pressure-flow relationship. The addition of washed red blood cells (RBCs) to physiological salt solution, but not the addition of plasma and platelets, restored the response to L-NAME. This effect of RBCs was not reproduced by increasing perfusate viscosity with dextran. These results suggest that, in the rabbit lung, NO is a determinant of PVR in the presence of blood. Moreover, that aspect of blood that permits the generation of NO appears to be related to the RBC and not to perfusate viscosity.

Hemoglobin and red blood cells alter the response of expired nitric oxide to mechanical forces

2000 ◽  
Vol 279 (6) ◽  
pp. H2947-H2953 ◽  
Author(s):  
John T. Berg ◽  
Steven Deem ◽  
Mark E. Kerr ◽  
Erik R. Swenson
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Venous Pressure ◽  
No Production ◽  
Mechanical Forces ◽  
Blood Flow Reduction ◽  
Lung Epithelial ◽  
Isolated Lungs

Expired nitric oxide (NOe) varies with hemodynamic or ventilatory perturbations, possibly due to shear stress- or stretch-stimulated NO production. Since hemoglobin (Hb) binds NO, NOe changes may reflect changes in blood volume and flow. To determine the role of blood and mechanical forces, we measured NOe in anesthetized rabbits, as well as rabbit lungs perfused with buffer, red blood cells (RBCs) or Hb following changes in flow, venous pressure (Pv), and positive end-expiratory pressure (PEEP). In buffer-perfused lungs decreases in flow and Pv reduced NOe, but NOe rose when RBCs and Hb were present. These findings are consistent with changes in vascular NO production, whose detection is obscured in blood-perfused lungs by the more dominant effect of Hb NO scavenging. PEEP decreased NOe in all perfused lungs but increased NOe in live rabbits. The NOe fall with PEEP in isolated lungs is consistent with flow redistribution from alveolar septal capillaries to extra-alveolar vessels and decreased surface area or a direct, stretch-mediated depression of lung epithelial NO production. In live rabbits, increased NOe may reflect blood flow reduction and decreased Hb NO scavenging and/or autonomic responses that increase NO production. We conclude that blood and systemic responses render it difficult to use NOe changes as an accurate measure of lung tissue NO production.

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