Effect of ischemia and reperfusion without airway occlusion on vascular barrier function in the in vivo mouse lung

被引:17
作者
Dodd-o, JM
Hristopoulos, ML
Faraday, N
Pearse, DB
机构
[1] Johns Hopkins Med Inst, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21287 USA
[2] Johns Hopkins Med Inst, Dept Med, Div Pulm & Crit Care Med, Baltimore, MD 21287 USA
关键词
pulmonary edema; vascular permeability; Evans blue dye; radiolabeled albumin; pulmonary artery; bronchial artery;
D O I
10.1152/japplphysiol.00456.2003
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Ischemia-reperfusion (I/R) lung injury causes increased vascular permeability and edema. We developed an in vivo murine model of I/R allowing measurement of pulmonary vascular barrier function without airway occlusion. The left pulmonary artery (PA) was occluded with an exteriorized, slipknotted suture in anesthetized C57BL/6J mice. The effect of ischemic time was determined by subjecting mice to 5, 10, or 30 min of left lung ischemia followed by 150 min of reperfusion. The effect of reperfusion time was determined by subjecting mice to 30 min of left lung ischemia followed by 30 or 150 min of reperfusion. Changes in pulmonary vascular barrier function were measured with the Evans blue dye (EBD) technique, dual-isotope radiolabeled albumin (RA), bronchoalveolar lavage (BAL) protein concentration, and wet weight-to-dry weight ratio (WW/DW). Increasing left lung ischemia with constant reperfusion time or increasing left lung reperfusion time after constant ischemic time resulted in significant increases in left lung EBD content at all times compared with both right lung values and sham surgery mice. The effects of left lung ischemia on lung EBD were corroborated by RA but the effects of increasing reperfusion time differed, suggesting binding of EBD to lung tissue. An increase in WW/DW was only detected after 30 min of reperfusion, suggesting edema clearance. BAL protein concentrations were unaffected. We conclude that short periods of I/R, without airway occlusion, increase pulmonary vascular permeability in the in vivo mouse, providing a useful model to study molecular mechanisms of I/R lung injury.
引用
收藏
页码:1971 / 1978
页数:8
相关论文
共 36 条
[1]   ATP-independent membrane depolarization with ischemia in the oxygen-ventilated isolated rat lung [J].
Al-Mehdi, AB ;
Zhao, GC ;
Fisher, AB .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1998, 18 (05) :653-661
[2]   Endothelial NADPH oxidase as the source of oxidants in lungs exposed to ischemia or high K+ [J].
Al-Mehdi, AB ;
Zhao, GC ;
Dodia, C ;
Tozawa, K ;
Costa, K ;
Muzykantov, V ;
Ross, C ;
Blecha, F ;
Dinauer, M ;
Fisher, AB .
CIRCULATION RESEARCH, 1998, 83 (07) :730-737
[3]   Protective effects of intravascular pressure and nitric oxide in ischemic lung injury [J].
Becker, PM ;
Buchanan, W ;
Sylvester, JT .
JOURNAL OF APPLIED PHYSIOLOGY, 1998, 84 (03) :803-808
[4]   SEPARATE EFFECTS OF ISCHEMIA AND REPERFUSION ON VASCULAR-PERMEABILITY IN VENTILATED FERRET LUNGS [J].
BECKER, PM ;
PEARSE, DB ;
PERMUTT, S ;
SYLVESTER, JT .
JOURNAL OF APPLIED PHYSIOLOGY, 1992, 73 (06) :2616-2622
[5]   LUNG REPERFUSION IN DOGS CAUSES BILATERAL LUNG INJURY [J].
BISHOP, MJ ;
CHI, EY ;
CHENEY, FW .
JOURNAL OF APPLIED PHYSIOLOGY, 1987, 63 (03) :942-950
[6]  
BISHOP MJ, 1986, AM REV RESPIR DIS, V134, P752
[7]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[8]   EVANS BLUE-DYE IN THE ASSESSMENT OF PERMEABILITY-SURFACE AREA PRODUCT IN PERFUSED RAT LUNGS [J].
DALLAL, MM ;
CHANG, SW .
JOURNAL OF APPLIED PHYSIOLOGY, 1994, 77 (02) :1030-1035
[9]   Effect of the NADPH oxidase inhibitor apocynin on ischemia-reperfusion lung injury [J].
Dodd-O, JM ;
Pearse, DB .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2000, 279 (01) :H303-H312
[10]   PATTERN OF INJURY AND THE ROLE OF NEUTROPHILS IN REPERFUSION INJURY OF RAT LUNG [J].
EPPINGER, MJ ;
JONES, ML ;
DEEB, M ;
BOLLING, SF ;
WARD, PA .
JOURNAL OF SURGICAL RESEARCH, 1995, 58 (06) :713-718