Normal adaptation of pulmonary arterial intima to extrauterine life in the pig: Ultrastructural studies

Department of Paediatric Cardiology, Institute of Child Health, Guilford Street, London, WCIN 1EH, U.K.
The Journal of Pathology (Impact Factor: 7.43). 05/1986; 149(1):55 - 66. DOI: 10.1002/path.1711490111


Adaptation of the pulmonary arterial intima was studied in injected lung specimens of 34 Large White pigs. Each type of pre- and intra-acinar artery was studied separately using transmission and scanning electron microscopy. Determination of the endothelial surface/volume ratio and volume densities of (1) endothelium and subendothelium. (2) endothelial cytoplasmic organelles and (3) subendothelial connective tissue elements yielded 6832 measurements which comprised a computerized database. At birth, endothelial cell morphology changed more rapidly and to a greater extent in peripheral than in proximal arteries. Endothelial surface/volume ratio increased (p < 0.0001). Fetal surface projections, junctional interdigitations and overlap became less evident. Adaptational changes were complete in three weeks. Between three weeks and adulthood a reduction in endothelial surface/volume ratio suggested cell growth. In the subendothelium the volume density of collagen and basement membrane and elastin increased (p<0.001). The internal elastic lamina, immature in all arteries at birth increased in thickness and integrity until in the adult, only in small muscular arteries did gaps between elastin profiles ensure frequent contact between endothelial and smooth muscle cells. At all ages regional differences in endothelial cell morphology were evident.

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    • "Pulmonary artery resistance is caused by both pulmonary arteries with SMC and pulmonary vessels without SMC or pulmonary vascular bed (Hall and Haworth 1986; Robert et al. 1998). However progressive reduction in pulmonary vascular resistance following birth is generally associated with histological changes within the pulmonary vascular bed, not those within pulmonary artery with SMC as discussed above (Hall and Haworth 1986). Robert et al. (1998) reported that no more than 50% of the total resistance is associated with vessels of less than 40 micron in their diameter. "
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    ABSTRACT: Pulmonary vascular resistance drops sharply within a few minutes after birth for the survival of neonates. A majority of this resistance is caused by "pulmonary vascular bed" or vessel lacking smooth muscle cells. Heparin is known to promote proliferation and development of endothelial cells and to subsequently decrease their overall vascular resistance, but its detailed features remained unknown. Therefore, in this study we treated neonatal rabbits with heparin, protamine (antagonist of heparin), or saline, and evaluated histopathological features of vascular endothelial cells using two different types of computer assisted image analysis, i.e., CAS200 and NIH image. These two systems detected the percentage of vascular endothelial area per fields (VA) and CD31-positive area per total area of tissue following subtraction of background stain. CD31 was used as an endothelial cell marker. Heparin treated rabbits were associated with significant decrement of pulmonary/systemic artery pressure (Pp/Ps) (21.0 +/- 6.0%) compared to protamine (29.9 +/- 6.1%) or saline (29.4 +/- 3.0%) treated animals. The values of VA obtained by the two image analyses (CAS200 and NIH image) were significantly increased in heparin treated animals (38.4 +/- 3.2% determined by CAS200 and 24.0 +/- 1.3% by NIH image) compared to protamine (30.2 +/- 3.9% and 19.2 +/- 1.8%) or saline (33.2 +/- 1.5% and 20.8 +/- 3.8%) treated animals on 14th day of treatment. The present study indicates that heparin accelerates pulmonary vascular bed development probably by increasing the number and volume of endothelial cells, which subsequently contributes to the decrease in pulmonary vascular resistance.
    The Tohoku Journal of Experimental Medicine 11/2005; 207(2):171-9. DOI:10.1620/tjem.207.171 · 1.35 Impact Factor
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    ABSTRACT: Hypoxemic respiratory failure in the term newborn is still an important cause of morbidity and mortality during the first month of extrau - terine life. The most common causes are meconium aspiration syndrome (MAS), hyaline membrane syndrome, pneumonia/sepsis and pulmonary hypoplasia with or without congenital diaphragmatic hernia. Most of these diseases can become complicated with persistent pulmonary hypertension, making their treatment difficult. The echocardiographic findings for the diagnosis of pulmonary hypertension include an elevated pressure of the pulmonary artery and extrapulmonary right -to-left shunting of blood at the foramen ovale and/or the ductus arteriosus. We made a review about prenatal growth and development of the pulmonary circulation and the differences between hypoxia and hypoxemia.
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