The Role of Red Blood Cells and Hemoglobin–Nitric Oxide Interactions on Blood Flow

2008 ◽  
Vol 38 (2) ◽  
pp. 125-126 ◽  
Author(s):  
Mark T. Gladwin ◽  
Rakesh P. Patel
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Red Blood Cells ◽  
Blood Cells

scholarly journals Role of membrane permeability and extracellular diffusion in nitric oxide transport to the red blood cells

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Prabhakar Deonikar ◽  
Mahendra Kavdia
Keyword(s):  
Nitric Oxide ◽  
Red Blood Cells ◽  
Membrane Permeability ◽  
Blood Cells

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.

scholarly journals Vaso-Occlusion in Sickle Cell Disease: Is Autonomic Dysregulation of the Microvasculature the Trigger?

2019 ◽  
Vol 8 (10) ◽  
pp. 1690 ◽  
Author(s):  
Saranya Veluswamy ◽  
Payal Shah ◽  
Christopher Denton ◽  
Patjanaporn Chalacheva ◽  
Michael Khoo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Sickle Cell Disease ◽  
Red Blood Cells ◽  
Sickle Cell ◽  
Blood Cells ◽  
Critical Role ◽  
Microvascular Blood Flow ◽  
Cell Disease ◽  
Hemoglobin S

Sickle cell disease (SCD) is an inherited hemoglobinopathy characterized by polymerization of hemoglobin S upon deoxygenation that results in the formation of rigid sickled-shaped red blood cells that can occlude the microvasculature, which leads to sudden onsets of pain. The severity of vaso-occlusive crises (VOC) is quite variable among patients, which is not fully explained by their genetic and biological profiles. The mechanism that initiates the transition from steady state to VOC remains unknown, as is the role of clinically reported triggers such as stress, cold and pain. The rate of hemoglobin S polymerization after deoxygenation is an important determinant of vaso-occlusion. Similarly, the microvascular blood flow rate plays a critical role as fast-moving red blood cells are better able to escape the microvasculature before polymerization of deoxy-hemoglobin S causes the red cells to become rigid and lodge in small vessels. The role of the autonomic nervous system (ANS) activity in VOC initiation and propagation has been underestimated considering that the ANS is the major regulator of microvascular blood flow and that most triggers of VOC can alter the autonomic balance. Here, we will briefly review the evidence supporting the presence of ANS dysfunction in SCD, its implications in the onset of VOC, and how differences in autonomic vasoreactivity might potentially contribute to variability in VOC severity.

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.

scholarly journals Role of oxygen‐dependent ATP release by red blood cells in metabolic regulation of blood flow

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Julia C Arciero ◽  
Timothy W. Secomb
Keyword(s):  
Blood Flow ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Metabolic Regulation ◽  
Atp Release

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.

Treatment with a Novel Dinitroazetidine, Abdnaz, Improves Nitrite Reductase Activity of Sickle Red Blood Cells

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 3246-3246 ◽  
Author(s):  
Marcel H.A.M. Fens ◽  
Sandra K Larkin ◽  
William L Fitch ◽  
Jan Scicinski ◽  
Bryan Oronsky ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Red Blood Cells ◽  
Normal Control ◽  
Sickle Cell ◽  
Nitrite Reductase ◽  
Blood Cells ◽  
Final Concentration ◽  
Blood Samples ◽  
No Release

Abstract Abstract 3246 Introduction Vaso-occlusion is a hallmark of sickle cell disease (SCD). Congestion of blood vessels by sickle red blood cells (RBC) is caused by hemoglobin polymerization (sickling), increased adhesion, and vasoconstriction due to a disregulated nitric oxide (NO) metabolism. NO generated from L-arginine by NO synthases plays a key role in vasodilation. Under hypoxia hemoglobin has been shown to be a potent alternative source of NO by reducing nitrite (NO2−). In SCD, modification of hemoglobin may reduce sickling and increase its ability to generate NO, and as such improve blood flow. In this study, we examined hemoglobin modification and consequent change in nitrite reductase capacity by 1-bromoacetyl-3,3-dinitroazetidine (ABDNAZ). This is a compound that has recently been described to bind to hemoglobin (Scicinski et al. Drug Met Disp. 2012) and has promising anticancer activity by altering blood flow in hypoxic tumors (Ning et al. Cancer Res. 2012). Method Blood samples from SCD patients and control blood from healthy volunteers was collected with IRB approval. Red blood cells were isolated and resuspended to physiological hemactocrit in HEPES buffered saline (HBS) containing 2% bovine serum albumin (BSA). Samples were incubated with ABDNAZ, hydroxyurea (HU) or iodoacetamide at a final concentration of 3 mM for 30 minutes at room temperature. Intact RBC, hemolysates or purified hemoglobin samples were exposed to a constant nitrogen (N2) flow (200 mL/minute) at 37°C in a tonometer. At time zero, sodium nitrite was added to a final concentration of 5 mM. The influx of NO2− into the RBC was measured using Griess reagent on supernatant samples. The gas outflow from the tonometer was collected in Mylar balloons at various time points, and NO released in the gas phase was measured using a Nitric Oxide Analyzer. Results Upon NO2− addition under deoxygenated conditions, influx in RBC was rapid. An equilibrium between supernatant and RBC was reached within 10 minutes and indicated active recruitment of RBC rather than a simple diffusion equilibrium. Release of NO from SCD patient RBC was increased compared to normal control (HbAA) RBC. Under these conditions, hemolysates with the identical hemoglobin concentration as compared to intact RBC showed a pronounced increase in NO release. Using purified hemoglobin NO release was reduced to 50% as compared to hemolysates. Blood samples from both normal control and sickle cell patients treated with ABDNAZ, showed a significant increase in NO release as compared to untreated samples. Iodoacetamide and HU treatment, described to increase NO (Gladwin et al. Br. J. Hematol. 2002), also showed increased NO release but at a markedly lower level as compared to ABDNAZ treatment. Conclusions Episodes of vaso-occlusion result in pain and organ damage in SCD. Local generation of NO will improve vasodilation, and is potentially beneficial. The novel compound ABDNAZ, currently in human clinical trials, greatly increases nitrite reductase capacity of hemoglobin, in both normal and SCD blood samples. Our results indicate that this agent improves NO release from RBC and suggests that modification of sickle patient blood by ABDNAZ in the presence of plasma nitrite should be considered as a potential therapeutic approach. Disclosures: Scicinski: RadioRx, Inc: Employment. Oronsky:RadioRx, Inc: Employment.

Role of Nitric Oxide on Papillary Blood Flow and Pressure Natriuresis

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pressure Natriuresis

scholarly journals Mathematical Models for Some Aspects of Blood Microcirculation

Symmetry ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1020
Author(s):  
Angiolo Farina ◽  
Antonio Fasano ◽  
Fabio Rosso
Keyword(s):  
Blood Flow ◽  
Mathematical Models ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Blood Rheology ◽  
Small Class ◽  
Small Vessels ◽  
Blood Microcirculation ◽  
Peculiar Behavior

Blood rheology is a challenging subject owing to the fact that blood is a mixture of a fluid (plasma) and of cells, among which red blood cells make about 50% of the total volume. It is precisely this circumstance that originates the peculiar behavior of blood flow in small vessels (i.e., roughly speaking, vessel with a diameter less than half a millimeter). In this class we find arteriolas, venules, and capillaries. The phenomena taking place in microcirculation are very important in supporting life. Everybody knows the importance of blood filtration in kidneys, but other phenomena, of not less importance, are known only to a small class of physicians. Overviewing such subjects reveals the fascinating complexity of microcirculation.

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