Pulmonary vasocostriction in response to pulmonary tumor emboli

Purpose: showing that there is vasocostriction element in pulmonary tumor emboli which it seems a major factor in the pulmonary hypertension resulted from the tumor emboli Methods: R side heart cather placed in a dyspnic breast cancer patient with normal CXR after 4 month of her bone marrow transpant we found that the patient has a pulmonary hypertension and the cytology from a blood sample from distal port was positive for malignant cells, adenasine constant infusion given to the patient withmeasurment to the hymodynamices Cardiac output, Pulmonary fascular resistant, mean pulmonary artery) As a base line before infusion and 2 minutes after 50μg/kg min and 2 minutes after the infusion at rate 200 μg/kg/min Results: we were able to show a reduction in pulmonary vascular resistent of 39% and increase in cardiac output by 14.8% Conclusions: in pulmonary tumor emboli there is increase in the the vessel reactivity which it seems a cotributing factor in our case and we demonestrate that by the response to adenosine. Clinical Implications: to our knowledge adenosine has not been used before in this setting.