ABSTRACT
Pulmonary hypertension is characteristic of several chronic pulmonary vascular diseases affecting humans, and can arise from vasoconstriction or as a response to altered vascular structure. A pulmonary vascular disease more common in humans is the adult respiratory distress syndrome (ARDS). In ARDS, major clinical manifestations, such as dyspnea and impaired gas exchange, arise from an injured pulmonary vasculature that allows fluid to accumulate in the lungs. Laboratory animals treated with high doses of Monocrotaline (MCT) also develop hepatic centrilobular necrosis and die within a few days as a result of acute liver injury. MCT- or Monocrotaline pyrrole (MCTP)-induced pulmonary changes are considered to be a useful model for human chronic pulmonary vascular injury; however, until relatively, much of the work reported on the model has been descriptive in nature. Gross observations can be made and several markers may be measured to determine the nature and/or extent of MCT- or MCTP-induced lung injury.
