Dr. Mark Thomas Gladwin M.D.
Critical Care Surgeon | Critical Care Medicine
Vmb Nhlbi Nih 10 Center Dr Building 10, Room 5- Bethesda MD, 20892About
Dr. Mark Gladwin is a critical care surgeon practicing in Bethesda, MD. Dr. Gladwin specializes in the needs of critically ill surgical patients. Critical care surgeons are experts in treating physiologic responses to tissue injury from trauma, burns, infections, acute inflammation, operation and more. They are also trained to know how such injuries interact with other diseases that a patient may have. As a critical care surgeon, Dr. Gladwin has a broad knowledge base and full understanding of the biology of the critically ill patient and the patients organ system functions.
Provider Details
Expert Publications
Data provided by the National Library of Medicine- The acute chest syndrome in sickle cell disease. Possible role of nitric oxide in its pathophysiology and treatment.
- Relative role of heme nitrosylation and beta-cysteine 93 nitrosation in the transport and metabolism of nitric oxide by hemoglobin in the human circulation.
- Disorders of ciliary motility.
- Effects of inhaled nitric oxide on regional blood flow are consistent with intravascular nitric oxide delivery.
- Regional cerebral hyperperfusion and nitric oxide pathway dysregulation in Fabry disease: reversal by enzyme replacement therapy.
- Nitric oxide therapy in sickle cell disease.
- Pulmonary complications of sickle cell anemia. A need for increased recognition, treatment, and research.
- Noninvasive determination of spatially resolved and time-resolved tissue perfusion in humans during nitric oxide inhibition and inhalation by use of a visible-reflectance hyperspectral imaging technique.
- Renal pathology in hemizygous sickle cell mice.
- Effects of iron nitrosylation on sickle cell hemoglobin solubility.
- Epidermal growth factor induces p11 gene and protein expression and down-regulates calcium ionophore-induced arachidonic acid release in human epithelial cells.
- Haemoglobin: NO transporter, NO inactivator or NOne of the above?
- Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease.
- Hydroxyurea induces fetal hemoglobin by the nitric oxide-dependent activation of soluble guanylyl cyclase.
- An emerging role for nitric oxide in sickle cell disease vascular homeostasis and therapy.
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Mark Gladwin
Vmb Nhlbi Nih 10 Center Dr Building 10, Room 5- -Bethesda, MD 20892Get Direction
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