A5012455824- Nitric Oxide and Endothelin Effects
- Neuroscience of respiration and sleep
- Hemoglobinopathies and Related Disorders
- Heart Rate Variability and Autonomic Control
- Hemoglobin structure and function
- Iron Metabolism and Disorders
- Erythrocyte Function and Pathophysiology
- Heme Oxygenase-1 and Carbon Monoxide
- Retinal Diseases and Treatments
- Artificial Intelligence in Healthcare and Education
- Biomedical and Engineering Education
- Retinal Development and Disorders
- Lysosomal Storage Disorders Research
- Electronic Health Records Systems
- Pregnancy and preeclampsia studies
United States Food and Drug Administration
2022
Cardinal Glennon Children’s Medical Center
2002
National Institutes of Health
1999-2001
Center for Clinical Research (United States)
2001
University of Vermont
2001
National Institute of Neurological Disorders and Stroke
2001
University of North Carolina at Chapel Hill
2001
National Institute of Diabetes and Digestive and Kidney Diseases
2000
National Heart Lung and Blood Institute
2000
To determine the relative contributions of endothelial-derived nitric oxide (NO) vs. intravascular nitrogen species in regulation human blood flow, we simultaneously measured forearm flow and arterial venous levels plasma nitrite, LMW-SNOs HMW-SNOs, red cell S-nitrosohemoglobin (SNO-Hb). Measurements were made at rest during regional inhibition NO synthesis, followed by exercise. Surprisingly, found significant circulating arterial-venous nitrite gradients, providing a novel delivery source...
Nitric oxide (NO) may be stabilized by binding to hemoglobin, nitrosating thiol-containing plasma molecules, or conversion nitrite, all reactions potentially preserving its bioactivity in blood. Here we examined the contribution of blood-transported NO regional vascular tone humans before and during inhalation. While breathing room air then with at 80 parts per million, forearm blood flow was measured 16 subjects rest after blockade synthesis N(G)-monomethyl-L-arginine (L-NMMA) followed...
To quantify the reactions of nitric oxide (NO) with hemoglobin under physiological conditions and to test models NO transport on hemoglobin, we have developed an assay measure NO-hemoglobin reaction products in normal volunteers, basal during inhalation. inhalation markedly raised total nitrosylated levels, a significant arterial-venous gradient, supporting role for delivery NO. The predominant species accounting this gradient is nitrosyl(heme)hemoglobin. breathing increases S-nitrosation...
Background Fabry disease is an X-linked lysosomal deficiency of α-galactosidase A that results in cellular accumulation galacto-conjugates such as globotriosylceramide, particularly blood vessels. It associated with early-onset stroke and kidney heart failure. Methods Results Using [ 15 O] H 2 O PET, we found increased resting regional cerebral flow without evidence occlusive vasculopathy or hypoperfusion. Because nitric oxide known to play important role vascular tone reactivity, studied...
Nitric oxide (NO) may be stabilized by binding to hemoglobin, nitrosating thiol-containing plasma molecules, or conversion nitrite, all reactions potentially preserving its bioactivity in blood. Here we examined the contribution of blood-transported NO regional vascular tone humans before and during inhalation. While breathing room air then with at 80 parts per million, forearm blood flow was measured 16 subjects rest after blockade synthesis NG-monomethyl-L-arginine (L-NMMA) followed...
Summary. Hydroxyurea therapy reduces the rates of vaso‐occlusive crisis in patients with sickle cell anaemia and recent data suggest that hydroxyurea treatment can generate nitric oxide (NO). Nitric has been proposed as a novel for disease via number pathways. We therefore sought to determine whether NO donor properties explore potential mechanisms by which production could be therapeutic. Venous blood was collected from 19 fasting patients, on chronic therapy, at baseline 2 4 h after single...
Nitric oxide (NO) inhalation has been reported to increase the oxygen affinity of sickle cell erythrocytes. Also, proposed allosteric mechanisms for hemoglobin, based on S-nitrosation β-chain cysteine 93, raise possibilty altering pathophysiology disease by inhibiting polymerization or increasing NO delivery tissue. We studied effects a 2-hour treatment, using varying concentrations inhaled NO. Oxygen affinity, as measured P50, did not respond NO, either in controls individuals with disease....
We have recently reported that nitric oxide inhalation in individuals with sickle cell anemia increases the level of NO bound to hemoglobin, development an arterial-venous gradient, suggesting delivery tissues. A recent model suggests oxide, addition its well-known reaction heme groups, reacts beta-globin chain cysteine 93 form S-nitrosohemoglobin (SNO-Hb) and SNO-Hb would preferentially release tissues thus modulate blood flow. However, we also determined primary hemoglobin adduct formed...