Date of Award
Master of Science
Dr. Karim Essani
Dr. Susan Stapleton
Dr. Luis H. Toledo-Pereyra
Masters Thesis-Open Access
Nitric oxide (NO) is involved in several metabolic pathways and physiological phenomena. The role of NO in inflammation after ischemia and reperfusion (I/R) is controversial. The early phases of inflammation include the leukocyte-endothelial (L/EC) cell interactions which have been divided in rolling, activation, adhesion and migration.
The first experiment was to demonstrate the role of NO in a model of renal I/R. We demonstrated that exogenous NO improves survival and renal function tests after renal I/R, while endogenous NO does not appear to be an important contributor to renal I/R. We also demonstrated that NO modulate the infiltration of neutrophils (migration) in postischemic damaged kidneys, by counting the neutrophils and by measuring the activity of myeloperoxidase in renal tissue. Finally, using the model of intravital microscopy, we demonstrated in a model of mesenteric I/R in the rat, that exogenous NO down-regulated the L/EC interactions (rolling and adhesion).
These results suggest that NO exerts a beneficial effect in I/R through its ability to down-regulate the rolling, adhesion and further migration of neutrophils into the ischemically damage tissue.
López-Neblina, Fernando, "The Role of Nitric Oxide in the Modulation of the Leukocyte-Endothelial Cell Interactions during Ischemia and Reperfusion" (1996). Masters Theses. 4500.