Restoration of pathological changes of emphysema by angiogenesis factors:experiment of rats

Abstract

To investigate whether intratracheal administration of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) restore the pulmonary function and pathology in emphysema, and research the mechanism of they restored pulmonary emphysema, and the pathogenesis of pulmonary emphysema. Twenty-four Wistar rats were randomized into the 4 equal groups: bFGF group [receiving a single intratracheal instillation of porcine pancreatic elastase (PPE) 250 U/kg, and 4 weeks later receiving intratracheal instillation of bFGF 400 U once a week for 3 weeks), VEGF group (receiving a single intratracheal instillation of PPE 250 U/kg, and 4 weeks later receiving intratracheal instillation of VEGF 2 microg once a week for 3 weeks), control group [receiving a single intratracheal instillation of PPE 250 U/kg, and 4 weeks later receiving intratracheal instillation of normal saline (NS) once a week for 3 weeks], and normal group (receiving intratracheal instillation of NS in above-mentioned pattern). Four weeks after treatment, arterial blood sample was collected from the abdominal aorta to undergo blood gas analysis for assessment pulmonary function, and then the rata were killed with their lungs taken out to undergo pathological examination. Immunohistochemistry was performed to detect the CD34, markers of pulmonary capillary endothelial cells. There were no significant differences in the artery blood gas analysis among the four groups (all P > 0.05). The levels of mean alveoli number (MAN) of the bFGF and VEGF groups were (43 +/- 8)/HP and (44 +/- 9)/HP] respectively, both significantly higher than that of the control group [(30 +/- 6)/HP, both P < 0.01]. The levels of mean linear intercept (MLI) of the bFGF and VEGF groups were (196 +/- 38) microm and (194 +/- 38) microm respectively, both significantly lower than that of the control group [(288 +/- 68) microm, both P < 0.01). the mean alveoli area (MAA) level of the bFGF and VEGF groups were (9856 +/- 1864) microm(2) and (9804 +/- 1929) microm(2) respectively, both significantly lower than that of the control group [(14,525 +/- 3408) microm(2), both P < 0.01]. The percentages of CD34(+) cells of the bFGF and VEGF groups were (3.7 +/- 1.3)% and (2.6 +/- 1.2)% respectively, both significantly higher than that of the control group [(0.8 +/- 0.7)%, both P < 0.05). bFGF and VEGF can restore the pathological changes of experimental emphysema. The damage of pulmonary capillary may play an important role in the pathogenesis of pulmonary emphysema.