Acinar arterial changes with chronic lung disease of prematurity in the surfactant era.
Because echocardiographic studies on infants with chronic lung disease (CLD) suggest that pulmonary hypertension (PH) may contribute to its severity, we studied acinar arterial walls in the following surfactant-era infants: controls (n=38): 22-41 weeks of gestational age (GA), exposed briefly to oxygen and positive pressure ventilation, died within 48 hr of birth; prolonged rupture of fetal membranes (PROM) and persistent pulmonary hypertension (PPHN) (n=17); and SCORE (integrated area under curve of average daily FiO2 x average daily MAP) groups (<20, 20-69, and 70-500; mild, moderate, and severe clinical lung disease, respectively, n=35): 23-30 weeks GA, lived 7-79 days. Lungs were stained for elastic tissue and smooth muscle actin. Vessels were assessed for percent of vessel circumference with smooth muscle, extent of elastic laminae in the walls, and percent arterial wall thickness (%AWT) at three levels: terminal to respiratory bronchiole transition (TRB), alveolar duct, and saccule. At the alveolar ductal and saccular levels, percent arterial wall thickness (%AWT) in mild CLD (SCORE < 20) was less than controls (P < 0.05) and those with more severe CLD (SCORE 70-500), indicating that normal postnatal arterial wall thinning may be delayed, or there is remodeling associated with increased %AWT. Severe CLD infants also had a significantly higher percent of circumferential actin than those with milder disease (SCORE < or = 69) and controls. In moderate and severe CLD, there was an increase in extent of the elastic laminae compared to controls and mild CLD. These changes were also significantly greater in PROM and PPHN infants compared to even severe CLD. We conclude that PH is a real possibility in severe CLD infants after discharge at 36 weeks. Grading the severity of CLD at discharge, and echocardiographic studies, may guide subsequent oxygen therapy.
Thibeault
Donald W
DW
Department of Pediatrics, Children's Mercy Hospital, Kansas City, Missouri 64108, USA. dthibeault@cmh.edu
Truog
William E
WE
Ekekezie
Ikechukwu I
II
D000199:Actins / Q000032:analysis; D001158:Arteries / Q000473:pathology*; D001997:Bronchopulmonary Dysplasia / Q000188:drug therapy / Q000473:pathology; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000473:pathology; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007233:Infant, Postmature; D007235:Infant, Premature, Diseases / Q000188:drug therapy / Q000473:pathology*; D008168:Lung / Q000098:blood supply* / Q000473:pathology*; D008171:Lung Diseases / Q000188:drug therapy / Q000473:pathology*; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009929:Organ Size; D010547:Persistent Fetal Circulation Syndrome / Q000473:pathology; D011663:Pulmonary Surfactants / Q000627:therapeutic use; D012121:Respiration, Artificial
D000199:Actins; D011663:Pulmonary Surfactants