The structure of the pulmonary trunk at different ages and in cases of pulmonary hypertension and pulmonary stenosis

Heath, Donald; Wood, Earl H.; DuShane, James W.; Edwards, Jesse E.

doi:10.1002/path.1700770216

Cited by 131 publications

(54 citation statements)

References 5 publications

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“…For example, tropoelastin and type I procollagen are expressed by smooth muscle cells within a thick, fibrous neointima composed of smooth muscle-like cells, macrophages and extracellular matrix, similar to the atherosclerotic lesions found in systemic arteries (1)(2)(3)(4). In contrast to systemic arteries, however, neointimal or atherosclerotic changes are rarely observed in normotensive elastic pulmonary arteries, even in the elderly (1) or in the presence of risk factors for systemic vascular atherosclerosis such as diabetes, tobacco smoke, or hypercholesterolemia (2). One explanation for the absence of neointimal and atherosclerotic lesions in normal pulmonary arteries is their low blood pressure rather than an intrinsic difference between pulmonary and systemic arteries (2,5,6).…”

Section: Introductionmentioning

confidence: 83%

The role of vascular injury and hemodynamics in rat pulmonary artery remodeling.

Tanaka

Schuster²,

Davis³

et al. 1996

J. Clin. Invest.

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Vascular remodeling in adult human elastic pulmonary arteries is characterized by diffuse neointimal lesions containing smooth muscle cells expressing extracellular matrix genes. Recent studies suggest vascular injury is needed to initiate remodeling and that growth factor mediators participate in the repair response. However, because neointimal formation is only observed in patients with pulmonary artery blood pressures approaching systemic levels, it has been hypothesized that systemic-like hemodynamic conditions are also necessary. To test that hypothesis, subclavian-pulmonary artery anastomoses were created in Sprague-Dawley rats under three different experimental conditions: no accompanying injury, or after monocrotaline or balloon endarterectomy injury.Pulmonary vascular remodeling was not induced by the subclavian-pulmonary artery anastomosis alone. A nonneointimal pattern of remodeling after mild monocrotalineinduced injury was converted into a neointimal pattern in the presence of the anastomosis. Neointima was also observed after severe, balloon endarterectomy-induced injury even in the absence of anastomosis. Tropoelastin, type I procollagen and TGF-␤ gene expression, and angiotensin converting enzyme immunoreactivity, was confined to the neointima resembling the pattern of gene expression and immunoreactivity in human hypertensive elastic pulmonary artery neointimal lesions. These observations introduce the concepts that the type of injury and the associated hemodynamic conditions can modify the elastic pulmonary artery response to injury.

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Section: Introductionmentioning

confidence: 83%

The role of vascular injury and hemodynamics in rat pulmonary artery remodeling.

Tanaka

Schuster²,

Davis³

et al. 1996

J. Clin. Invest.

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“…In the fetus, the configuration of the elastic fibers in the pulmonary trunk is similar to that of the aorta. During normal postnatal development marked differences in the arrangement of the network of elastic fibers between the aorta and pulmonary artery are observed (43 …”

Section: Pulmonary Arterymentioning

confidence: 99%

Persistence of the fetal pattern of tropoelastin gene expression in severe neonatal bovine pulmonary hypertension.

Stenmark

Durmowicz²,

Roby³

et al. 1994

J. Clin. Invest.

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Neonatal hypoxic pulmonary hypertension causes increases and spatial changes in tropoelastin expression in pulmonary arteries. However, it is not clear if this is due to recruitment of quiescent smooth muscle cells (SMC) into an elastin-producing phenotype or persistence of the fetal pattern of tropoelastin gene expression. We evaluated the distribution and relative concentration of tropoelastin mRNA in intralobar pulmonary arteries from late gestation fetuses and in animals exposed to hypobaric hypoxia (430 mmHg) from birth for 1, 3, 7, or 14 d, as well as in age-matched and adult room air-breathing controls. In situ hybridization demonstrated that tropoelastin mRNA was distributed throughout the entire radius of the pulmonary vessel wall in the fetus and newborn calf. By 15 d of age, only cells in the inner third of the media expressed tropoelastin mRNA, and by adulthood no tropoelastin mRNA was detected in the vessel wall. These findings demonstrated that tropoelastin expression shuts off in a spatially specific pattern, moving from the abluminal to the luminal side of the medial in the neonatal pulmonary artery when pressures and resistance are falling. In the aorta of 15-d-old calves, tropoelastin mRNA expression was seen equally throughout the media, indicating tissue-specific regulation of elastin in the neonatal period. In contrast, intralobar pulmonary arteries from calves exposed to hypoxia, which prevented the normal postnatal decline in pulmonary artery pressure, maintained the fetal pattern and levels of tropoelastin mRNA expression at all time points. Thus, rather than causing a recruitment of SMC into an elastin-producing phenotype, neonatal pulmonary hypertension caused a persistence of the fetal pattern of tropoelastin expression in medial SMC. Cell-free translation showed that the same tropoelastin isoforms were made by mRNA from control and hypertensive calves and, unlike the ligamentum nuchae, did not change during the transition from fetal to neonatal life. We conclude that pulmonary hypertension in the neonate perturbs the normal postpartum repression of tropoelastin expression resulting in a persistence of the fetal spacial and isoform patterns of tropoelastin gene expression. (J. Clin. Invest. 1994.

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“…This is nicely illustrated also by comparing the ascending aorta and the pulmonary trunk. During the gestational period-in general terms--left ventricular output is less than that of the right ventricle, but these differences gradually increase and at the time of birth both ascending aorta and pulmonary trunk have almost similar diameters and a similar configuration of elastin lamellae [12,13].…”

Section: Commentmentioning

confidence: 99%

Morphologic features of the normal aortic arch in neonates, infants, and children pertinent to growth

Machii

Becker

1997

The Annals of Thoracic Surgery

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The structure of the pulmonary trunk at different ages and in cases of pulmonary hypertension and pulmonary stenosis

Cited by 131 publications

References 5 publications

The role of vascular injury and hemodynamics in rat pulmonary artery remodeling.

The role of vascular injury and hemodynamics in rat pulmonary artery remodeling.

Persistence of the fetal pattern of tropoelastin gene expression in severe neonatal bovine pulmonary hypertension.

Morphologic features of the normal aortic arch in neonates, infants, and children pertinent to growth

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