gastrin-releasing-peptide and Hypertension--Pulmonary

The aim of the study was to see if there was any correlation between the histopathology, ultrastructure, pulmonary endocrinology and clinical manifestations of end-stage primary pulmonary hypertension. Twenty patients undergoing heart-lung transplantation for the disease were studied. The nature and duration of symptoms and signs, results of haematological, electrocardiographic, radiographic, echocardiographic and haemodynamic studies, and the response of patients to vasodilators were compared with data from histopathological and ultrastructural study of lungs removed at transplantation. Length of clinical history and clinical evidence of severe disease were not necessarily associated with advanced histopathology, nor did the presence of small, contracted muscular pulmonary arteries imply responsiveness to vasodilators. Numbers of gastrin-releasing peptide-containing pulmonary endocrine cells were greater in lungs in which there was activity of myofibroblasts in pulmonary arterial vessels, and correlated negatively with mean pulmonary artery pressure and pulmonary artery systolic pressure. Whereas the prognosis of primary pulmonary hypertension cannot as yet be defined by other than its clinical manifestations, intimal proliferation as well as vasoconstriction may be important in its pathogenesis. The release of gastrin-releasing peptide from pulmonary endocrine cells may possibly be involved in this process.

Topics: Adolescent; Adult; Calcitonin; Child; Child, Preschool; Female; Gastrin-Releasing Peptide; Gastrins; Heart-Lung Transplantation; Humans; Hypertension, Pulmonary; Lung; Male; Middle Aged; Peptides; Vasodilator Agents

The rôle of the endocrine cells which populate the airways of the lung is uncertain, although it has been suggested that one of their functions might be to regulate the pulmonary vasculature. We have studied the number, content and distribution of these cells in 26 pairs of lungs removed during heart-lung transplantation for the treatment of pulmonary hypertension of various causes, none of which were characterized by plexogenic arteriopathy. In comparison with the controls, there were no differences in the number, content or distribution of these cells, although in two cases of recurrent pulmonary thromboembolism they were aggregated into abnormal disorderly clusters.

Topics: Adult; Biomarkers; Calcitonin; Gastrin-Releasing Peptide; Humans; Hypertension, Pulmonary; Lung; Neurosecretory Systems; Peptides; Phosphopyruvate Hydratase