Norberto C. Gonzalez, M.D.

Professor
Universidad Nacional de La Plata, Argentina, 1962

Publications:PubMed Publications

Research Focus

Systemic oxygen transport during exerciese. Acclimatization to hypoxia.

Research Interests

My research centers on the mechanisms of adaptation of intact organisms to environmental hypoxia. Environmental hypoxia typically occurs during exposure to altitude and results in alterations in systemic O2 transport  and limitations in exercise capacity. Individual that ascend to altitude rapidly may develop acute altitude illnesses such as acute mountain sickness, high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE). Acclimatized individuals, or persons indigenous to high altitude may develop chronic mountain sickness, or Monge’s disease, which is characterized by excessive polycythemia. 

My laboratory has been involved in studies directed to determine the mechanisms for the limitations in systemic O2 transport during maximal exercise in acute and chronic hypoxia, using a model which allowed the characterization of the various steps in systemic O2 transport from the environment to the tissue capillary.

A second line of research is the role of inflammation in the pathophysiology of acute illnesses of altitude. Recent studies in collaboration with Dr. John Wood have shown that rats and mice exposed to hypoxia develop a rapid and ubiquitous inflammatory response characterized by increased ROS and reduced NO levels in various microcirculatory beds, activations of perivascular mast cells, leukocyte recruitment and increased vascular permeability. If the animals are maintained in hypoxia for 2-3 weeks, the inflammation disappears and the animals do not demonstrate increased in inflammatory markers if exposed to even more severe hypoxia.

Characteristics of hypoxia-induced inflammation

Current efforts are directed to test the hypothesis that the systemic inflammation of hypoxia Is triggered by an agent released from a distant site and transported by the circulation.  This agent would initiate the inflammation by sctivating perivascular mast cells.