[Restoration of pathological changes of emphysema by angiogenesis factors: experiment of rats].
OBJECTIVE
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.


METHODS
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.


RESULTS
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).


CONCLUSIONS
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.
Li
Bao-ping
BP
Department of Cardiothoracic Surgery, Second Affiliated Hospital of Shanxi Medical University, Taiyuan 030001, China.
Zhao
Xiao-jian
XJ
Song
Yong-ming
YM
Zhang
Lei
L
Lu
Peng-yan
PY
Liu
Zhuo-la
ZL
Ma
Jie
J
D000818:Animals; D004195:Disease Models, Animal; D016222:Fibroblast Growth Factor 2 / Q000627:therapeutic use*; D008168:Lung / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D011656:Pulmonary Emphysema / Q000188:drug therapy* / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D042461:Vascular Endothelial Growth Factor A / Q000627:therapeutic use*
D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2