Platelet endothelial cell adhesion molecule-1 and capillary loading in premature infants with and without chronic lung disease.
It was our objective to quantify platelet endothelial cell adhesion molecule-1 (PECAM-1) by immunohistochemistry in control infants of 22-50 weeks postconceptual age, and to correlate it with varying degrees of neonatal chronic lung disease (CLD). We tested the hypothesis that the density of PECAM-1 staining will positively correlate with increasing gestational age (GA) and the inflammatory process in CLD. A library of postmortem lung tissue of infants receiving ventilator care was accessed. The population consisted of 35 control infants exposed briefly to oxygen and positive pressure ventilation, and 31 infants who were 23-30 weeks GA with mild to severe CLD. A monoclonal anti-human PECAM-1 antibody was used to stain 5-microm paraffin sections. The slides were viewed at a magnification of x 40 by a blinded examiner. Twenty consecutive fields from standardly expanded tissue samples were viewed, and the volume density of PECAM-1 (V(V PECAM)) per parenchyma was measured, using point counting. In addition, 1-microm sections from 15 controls and 5 infants with CLD were stained with Toluidine blue and viewed under oil at a magnification of x 100, and the volume density of capillaries (V(V CAP)) and capillary load (CL) were calculated. The V(V PECAM) increased significantly with GA in controls (r = 0.72, P < 0.001). There was no relationship between V(V PECAM) and severity of CLD. Both V(V CAP) and CL increased significantly with GA (r = 0.93, P < 0.001; r = 0.94, P < 0.001, respectively). The infants with CLD had a normal or increased V(V CAP) and CL compared to controls. In summary, V(V PECAM), V(V CAP), and CL increased significantly with gestational age in control infants, but the postconceptional age range in CLD infants was too short to determine whether the V(V PECAM) changed. Infants with CLD had normal or increased V(V CAP) and CL compared to controls. The PECAM-1 immunostain does not appear to be a sensitive method for assessing capillary density in infants with CLD. These findings of normal or increased capillary load may represent a vascular adaptation for the lack of secondary septation and decreased surface area in CLD.
Olsen
Steven L
SL
Section of Neonatology, Department of Pediatrics, Children's Mercy Hospitals and Clinics, UMKC School of Medicine, 2401 Gillham Road, Kansas City, MO 64108, USA.
Thibeault
Donald W
DW
Mabry
Sherry M
SM
Norberg
Michael
M
Truog
William E
WE
D000367:Age Factors; D002196:Capillaries / Q000196:embryology; D002908:Chronic Disease; D005314:Embryonic and Fetal Development; D005865:Gestational Age; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007231:Infant, Newborn; D007234:Infant, Premature / Q000378:metabolism*; D007235:Infant, Premature, Diseases / Q000378:metabolism* / Q000473:pathology; D008168:Lung / Q000098:blood supply / Q000196:embryology; D008171:Lung Diseases / Q000378:metabolism* / Q000473:pathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism*; D012720:Severity of Illness Index
D019408:Platelet Endothelial Cell Adhesion Molecule-1