ABSTRACT
BACKGROUND: Lung pericytes are important constituent cells of blood-air barrier in pulmonary microvasculature. These cells take part in the control of vascular contractility and permeability. In this study, it was hypothesized that change of lung pericytes might be attributable to pathologic change in microvasculature in acute lung injury. The purpose of this study was how hypoxia change proliferation and genetic expression in lung pericytes. METHODS: From the lungs of several Sprague-Dawley rats, performed the primary culture of lung pericytes and subculture. Characteristics of lung pericytes were confirmed with stellate shape in light microscopy and immunocytochemistry. 2% concentration of oxygen and 200muM CoCl2 were treated to cells. Tryphan blue method and reverse transcription-polymerase chain reaction were done. RESULTS: 1. We established methodology for primary culture of lung pericytes. 2. Hypoxia inhibited cellular proliferation in pericytes. 3. Hypoxia could markedly induce vascular endothelial growth factor(VEGF) and smad-2. 4. Hypoxia-inducible factor-1alpha (HIF-1alpha)was also induced by 2% oxygen. CONCLUSION: Viability of lung pericytes are inhibited by hypoxia. Hypoxia can stimulate expression of hypoxia-responsive genes. Pericytic change may be contributed to dysfunction of alveolar-capillary barrier in various pulmonary disorders.
Subject(s)
Acute Lung Injury , Hypoxia , Blood-Air Barrier , Cell Proliferation , Immunohistochemistry , Lung , Microscopy , Microvessels , Oxygen , Pericytes , Permeability , Rats, Sprague-Dawley , Vascular Endothelial Growth Factor AABSTRACT
A 30 year-old women who had had moderately advanced pulmonary tuberculosis and taken antituberculosis regimens including rifampicin was admitted with the symptoms of petechiae on the trunk and extremities and gum bleeding. The thrombocytopenic purpura appeared 20 days after the treatment with rifampicin, and which was rapidly improved with discontinuation of the drug. The diagnosis was confirmed by relapse of thrombocytopenia after retreatment with rifampicin. The paper presents a patient with thrombocytopenia induced by rifampicin and a brief review of pertinent literature.