Adventitial Remodeling Elastin and Collagen

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Stenmark et al. (43) took newborn calves to a simulated high altitude of 4,300 m and observed severe pulmonary hypertension with right-to-left shunting owing to the rapid development of suprasystemic levels of pulmonary artery pressure. There was striking medial hypertrophy and remarkable proliferation of a dense adventitial sheath that, in large vessels, was sometimes seen to exhibit neovascularization (Fig. 1). Hypoxiainduced adventitial fibroblast proliferation has been related to protein kinase (11). The contribution ofthe extensive vaso vasorum of the adventitia has been recently investigated (12). Stem cells have been identified in these vessels which have the capacity to differentiate into both endothelial as well as smooth muscle cells and may play a critical role in the structural remodeling that is associated with hypoxia (12). Studies have shown striking synthesis of elastin in the pulmonary arteries of these neonatal calves (36). There may be a role for IGF-1, as increased expression of this growth factor stimulates elastin synthesis in cultured vascular cells (14), as does TGF-B (25). Studies in the piglet by Allen and Haworth (1) showed that when the animal is subjected to hypoxia from birth, the fetal medial musculature does not regress, but connective tissue synthesis is not stimulated. When hypoxic exposure begins at 3 days of age, however, that is, after the fall in pulmonary vascular resistance and the regression of the fetal musculature, neosynthesis of elastin is apparent.

Figure 1. A: An artery from the lung of a 2-week-old calf raised at a simulated altitude of 4,300 m from birth. Systolic PAP was 100 mmHg. There is marked medial hypertrophy and adventitial thickening with neovascularization (x400). B and C: In situ hybridization localization of tropoelastin mRNA in control and hypertensive vessels from neonatal calves. White staining over areas indicates tropoelastin mRNA labeling. In normotensive vessels (B), labeled cells (35S-labeled T66-T7) were confined to the inner media. Minimal signal is noted in the outer vessel wall. In vessels from hypertensive animals (14 days of hypoxia) (C), intense autoradiographic signal was observed throughout the media, albeit in a patchy distribution (Modified from Ref. 36).

Figure 1. A: An artery from the lung of a 2-week-old calf raised at a simulated altitude of 4,300 m from birth. Systolic PAP was 100 mmHg. There is marked medial hypertrophy and adventitial thickening with neovascularization (x400). B and C: In situ hybridization localization of tropoelastin mRNA in control and hypertensive vessels from neonatal calves. White staining over areas indicates tropoelastin mRNA labeling. In normotensive vessels (B), labeled cells (35S-labeled T66-T7) were confined to the inner media. Minimal signal is noted in the outer vessel wall. In vessels from hypertensive animals (14 days of hypoxia) (C), intense autoradiographic signal was observed throughout the media, albeit in a patchy distribution (Modified from Ref. 36).

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