PMID- 15569452
OWN - NLM
STAT- MEDLINE
DCOM- 20051114
LR  - 20061115
IS  - 0376-2491 (Print)
IS  - 0376-2491 (Linking)
VI  - 84
IP  - 19
DP  - 2004 Oct 2
TI  - [Dynamic change of apoptosis of alveolar cells in ischemia-reperfusion induced 
      pulmonary injury: an experimental study with rats].
PG  - 1597-600
AB  - OBJECTIVE: To observe the dynamic changes of alveolar apoptosis in 
      ischemia-reperfusion (IR) induced pulmonary injury, and to evaluate the roles of 
      these two cell death styles, apoptosis and necrosis, in the progress of lung 
      function deterioration in pulmonary IR injury. METHODS: Fifty-four Sprague-Dawley 
      rats were made ischemia/reperfusion models by ischemia and reperfusion in situ in 
      single lung. Thirty-six of the 54 rats in the experimental group were re-divided 
      into 6 equal subgroups to undergo detection of partial pressure of oxygen (PaO2) 
      of blood in left atrium, detection of lung tissue wet weight/dry weight ratio, 
      histology of lung by light microscope, examination of ultrastructural changes of 
      cells by transmission electron microscopy, and quantitative detection of 
      apoptotic cells in the right middle lobe by terminal deoxynucleotidyl 
      transferase-mediated dUTP nick end labeling (TUNEL) 0 h, 0.5 h, 1 h, 2 h, 6 h, 
      and 12 h respectively after the reperfusion (subgroups R0, R(0.5), R1, R2, R6, 
      and R12). Another 18 rats in the experimental group were re-divided into 3 
      subgroups of 6 rats to undergo insertion of venous catheter into the main 
      pulmonary artery via right ventricle to perfuse trypan blue so as to evaluate the 
      cell death degree. The death index was observed under light microscope and the 
      necrosis index was indirectly calculated by the equation: death index = apoptotic 
      index + necrosis index. Thirty-six rats underwent sham operation. Twelve rats 
      were used as preoperative blank controls. RESULTS: Proliferation of alveolar type 
      II, but not alveolar type I cell, accompanied by ultrastructural morphological 
      changes were seen 1 h, 2 h, and 6 h after reperfusion, the most prominently 2 h 
      after reperfusion. Apoptotic index was elevated since 1 h after reperfusion, and 
      peaked 2 h after reperfusion. Statistical analysis indicated that, compared with 
      apoptotic index, the necrotic index was of more prominent correlation with blood 
      oxygen partial pressure and wet/dry weight ratio. CONCLUSION: Alveolar apoptosis 
      occurs in the early stage of reperfusion, and becomes the most prominent 2 h 
      after reperfusion. Most apoptotic cells are alveolar type II cells. In the two 
      styles of cell death in pulmonary IR injury, alveolar necrosis is more 
      prominently correlated with progress of lung function deterioration.
FAU - Zhang, Sai
AU  - Zhang S
AD  - Thoracic Cardiovascular Department, the Second Affiliated Hospital, School of 
      Medicine, Zhejiang University, Hangzhou 310009, China.
FAU - Chen, Ru-kun
AU  - Chen RK
FAU - Lin, Min
AU  - Lin M
FAU - He, Xue-ming
AU  - He XM
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhonghua Yi Xue Za Zhi
JT  - Zhonghua yi xue za zhi
JID - 7511141
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Female
MH  - Lung/*blood supply/pathology
MH  - Male
MH  - Pulmonary Alveoli/*pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*pathology
EDAT- 2004/12/01 09:00
MHDA- 2005/11/15 09:00
CRDT- 2004/12/01 09:00
PHST- 2004/12/01 09:00 [pubmed]
PHST- 2005/11/15 09:00 [medline]
PHST- 2004/12/01 09:00 [entrez]
PST - ppublish
SO  - Zhonghua Yi Xue Za Zhi. 2004 Oct 2;84(19):1597-600.