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Brief Program History

​     In 1965, Dr. Robert Grover initiated a line of investigation into the pathogenesis of hypoxic pulmonary hypertension in both humans and cattle at high altitude.  His questions were directed at elucidating the causes and consequences of hypoxic pulmonary vasoconstriction and vascular remodeling. To accomplish his goals he founded, at about the same time, the Cardiovascular Pulmonary (CVP) Research Laboratory, where under his guidance, a talented group of physicians and basic scientists were assembled thus establishing the interdisciplinary and collaborative working environment that continues to this day.  In 1975, the CVP Research Laboratory received its first research support through the Program Project Grant, “Adaptations to Hypoxia”. At the program’s inception, the major areas of investigation encompassed the breadth of adaptations to hypoxia, including studies of pulmonary hypertension, pulmonary microvascular permeability, systemic circulatory responses, control of ventilation, polycythemia, and cardiac hypertrophy.  In the years since its inception the CVP laboratory and the program project itself have evolved into a group whose focus is on the pathophysiology of the pulmonary circulation not only under hypoxic conditions, but in response to other stresses as well. The bovine model of severe hypoxic pulmonary hypertension has been a mainstay of the laboratory since its inception, and continues to be used extensively, even today. In addition, the laboratory has, since its earliest days, also used many animal model systems to interrogate questions related to pulmonary vascular disease. They have included hypoxic mice, rats, rabbits, sheep, and even yaks. Extensive use of the monocrotaline rat model of PH has been ongoing in the laboratory for more than 25 years. Members of the laboratory were instrumental in developing the now commonly used Sugen+Hypoxia model of PH. We have also made extensive use of numerous transgenic mouse strains in past and ongoing studies. The diversity of the systems used to answer questions regarding inflammation in PH is a significant strength in the Program. The Program investigate of the commonality of macrophage, and probably fibroblast, involvement in the different models, and likely human varieties, of PH, while allowing us to address exciting differences in pathways leading to these central activities. These investigations lend themselves to address the key aspect of inflammation persistence: The positive feedback signaling between the macrophage and fibroblasts, including intracellular processes common to both cells, is a likely candidate for the inability of the inflammation to undergo its normal resolution processes.

     Though many of the faces participating in the program have changed over the years, the philosophy of collaborative, innovative research using many different model systems (large and small animals, isolated lungs, cultured primary vascular cells) and expertise available has not. The CVP laboratory has and continues to remain a vital area for collaboration and training students of all levels in physiology, pulmonary medicine (adult and pediatric) and cardiology within the University of Colorado. It is home to investigators with expertise in biomechanics, genetics, cell signaling and stem cell biology. It also provides a “home” for a T32 Training Grant entitled “Translational Pulmonary Vascular Biology” (PI- Kurt Stenmark).

     Over the past 40 years program’s research activities have resulted in more than 1000 publications.  Its past members/trainees include leaders in lung and lung vascular research at prestigious institutions around the country and include Ken Weir, Sharon Rounds, John Newman, Norbert Voelkel, Ivan McMurtry, Marc Gillespie, Troy Stevens, Nick Morrell, Karen Fagan, and James West, among many others.