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  1. Lung diseases
  2. Pulmonary heart disease
  3. Pulmonary arterial hypertension
  4. 4th Edition
  5. Lung disease: MedlinePlus Medical Encyclopedia

Davidson's Principles and Practice of Medicine. Philadelphia, PA: Elsevier Ltd; chap Harron, Jr.

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Editorial team. Lung disease. There are three main types of lung disease: Airway diseases -- These diseases affect the tubes airways that carry oxygen and other gases into and out of the lungs. They usually cause a narrowing or blockage of the airways. Airway diseases include asthma , COPD and bronchiectasis. People with airway diseases often say they feel as if they're "trying to breathe out through a straw. Scarring or inflammation of the tissue makes the lungs unable to expand fully restrictive lung disease. This makes it hard for the lungs to take in oxygen and release carbon dioxide.

People with this type of lung disorder often say they feel as if they are "wearing a too-tight sweater or vest. Pulmonary fibrosis and sarcoidosis are examples of lung tissue disease.

Lung circulation diseases -- These diseases affect the blood vessels in the lungs. They are caused by clotting, scarring, or inflammation of the blood vessels. They affect the ability of the lungs to take up oxygen and release carbon dioxide. Vasculogenesis is the differentiation and segregation of angioblasts within the mesenchyme, which forms early vascular channels arteries, veins, and lymphatics , depending on local influences from the epithelium and the mesenchyme. The lung mesenchyme is the embryonic origin of the distal vasculature, which develops by angiogenesis.

Angiogenesis is the formation of new vessels from preexisting vascular channels by proliferation and migration of endothelial cells at the tips, which form multiple capillary sprouts. Abnormal maturation or maturational arrest in pulmonary arterial development is reflected in functional derangement that can appear in the newborn period.

Lung diseases

Persistent pulmonary hypertension of the newborn PPHN has been reported in association with pulmonary arterial maturational arrest at week 5 of gestation. Multiple factors influence development and growth of pulmonary vasculature in utero, including growth factors. Growth factors such as vascular endothelial growth factor 2 and fibroblast growth factor 3 appear to be responsible for orderly growth and branching morphogenesis of blood vessels. Quantity, timing, and location are critical determinants of the net effects of these agents. The mechanical stress that endothelial cells must withstand may be the predominant force responsible for development of large vessels after onset of circulation.

In the normal fetal and term lung, fully muscularized thick-walled preacinar arteries extend to the level of terminal bronchioles, whereas the intra-acinar arteries i.

Pulmonary heart disease

Arteries at alveolar ducts and alveolar walls are nonmuscular. Preacinar arteries in the fetus late in gestation and in the newborn have thicker coats of smooth muscle relative to the arterial diameter than do similar arteries in adults, although the fetus actually has less distal extension of smooth muscle in smaller arteries than do older children or adults. Increased muscularization of the pulmonary arteries has been described in infants with severe meconium aspiration syndrome MAS with PPHN. In utero ductal ligation 1 to 2 weeks prior to delivery results in severe PPHN at birth associated with distal extension of vascular smooth muscle in newborn lambs 10 Figure similar to the changes seen in human infants dying with severe PPHN.

Figure 48—1 Diagrammatic representation of a normal pulmonary artery from a term newborn infant showing a fully muscular media to the level of the terminal and respiratory bronchiole. A partial muscular layer extends further distally but the terminal portion of the arterial tree is devoid of smooth muscle. A pulmonary artery in an infant with severe persistent pulmonary hypertension of the newborn shows an increase in the thickness of the muscular layer and distal extension of muscle. Figure 48—2 Histology hematoxylin and eosin stain showing increased muscularization surrounding pulmonary arteries blue arrow following antenatal ductal ligation in lambs resulting in persistent pulmonary hypertension of the newborn B.

Control twin lamb A with a normal pulmonary artery red arrow is shown for comparison. The cartoon C shows increased muscularization and distal extension of muscle in persistent pulmonary hypertension of the newborn.

Pulmonary arterial hypertension

Oxygenated blood Pa O 2 approximately 30 to 40 mm Hg returning from the placenta in the umbilical vein 11 splits in the liver with slightly more than half passing through the ductus venosus to the inferior vena cava IVC. The oxygenated blood streams along the medial aspect of the IVC as it enters the right atrium Figure Approximately two thirds of the IVC flow is directed toward the foramen ovale by the eustachian valve and the septum primum and enters the left atrium.

The remaining third of the IVC flow mixes with the blood from the superior vena cava and enters the right ventricle. The majority of the right ventricular RV output enters the ductus arteriosus and the descending aorta. A small portion enters the lungs via the pulmonary arteries.

Figure 48—3 Fetal circulation showing the shunting of blood at the ductus venosus, foramen ovale, and ductus arteriosus. The fetal pulmonary circulation fulfills a unique function. The distribution of combined ventricular output, measured in fetal lambs ranging from 60 to days gestational age, indicates that the lungs receive only about 3.

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  5. The lung increases in weight by sixfold from midgestation to term, and the number of pulmonary vessels increases more than tenfold. However, Qp remains relatively constant when corrected for wet lung weight with advancing gestation. Low oxygen tension and various mediators play a crucial role in maintaining elevated fetal PVR. Conversely, increasing oxygen tension does not change PVR before days of gestation, but it decreases resistance markedly and increases blood flow to normal newborn levels at days of gestation.

    Arachidonic acid metabolites are some of the most powerful vasoconstrictors known. Of these compounds, HETE acids have been shown to constrict pulmonary circulation in newborn piglets. Leukotrienes are formed from arachidonic acid through the 5-lipooxygenase pathways. Lipoxygenase activity has been demonstrated in human fetal lung as early as 12 to 18 weeks of gestation.

    It is possible that they play a role in pathologic states such as hypoxia or inflammation. Endothelins ETs are residue peptides 30, 31 whose role in regulating vascular tone and vasomotor responses has been studied intensively in the past decade.

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    ET-1 synthesized by vascular endothelial cells is a potent vasoconstrictor, 32 and its effects in both animal and human studies vary with the tone of the pulmonary vessels, dose of ET-1, and the maturation of vessels. Both ET-1 and ET-2 have been shown to dilate the fetal normally high tone pulmonary vasculature and constrict the bed when the tone is reduced by ventilation. In contrast, infusion of big ET-1, the precursor of ET-1, into fetal lambs causes sustained pulmonary vasoconstriction, 36 suggesting that this might be the predominant effect of endogenous ET Selective blockade of the ET A receptor causes fetal pulmonary vasodilation.

    It is possible that prenatally, endogenous ET-1 primarily stimulates ET A receptors to cause vasoconstriction and that ET B receptors are less active in fetal life. Figure 48—4 Endothelin and nitric oxide pathways in pulmonary arterial endothelial and smooth muscle cells. The first stage of transitional circulation is essentially a fetal pulmonary circulation that is characterized by high pressure and low flow because of both passive and active elevation of PVR Figure , A.

    Pulmonary Circulation Diseases and Their Treatment, Fourth Edition

    The passive resistance most likely is related to compression of pulmonary capillaries by fetal lung liquid, but there is also a high degree of active vasomotor tone resulting from various mediators and hypoxic stimuli. Thus PVR exceeds systemic vascular resistance SVR , resulting in right atrial and ventricular pressures exceeding left atrial and ventricular pressures. High PVR results in right-to-left shunting of blood across the foramen ovale, and most of the blood ejected by the right ventricle flows across the ductus arteriosus into the descending aorta. Persistence of elevated PVR after birth without the benefit of placental oxygenation results in the profound hypoxemia that characterizes PPHN.

    Figure 48—5 Transitional circulation. Fetal circulation A is characterized by high pulmonary vascular resistance PVR , low pulmonary blood flow, and low systemic vascular resistance SVR. After birth, with the clamping of the umbilical cord, low resistance placental circulation is removed and SVR increases and with pulmonary vasodilation, PVR decreases B.

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    During the first few hours of postnatal life, morphologic changes occur in the pulmonary arterial endothelial cells and smooth muscle cells. These changes contribute to further reduction in PVR C. The second stage of normal transition is accomplished when the fluid-filled fetal lungs are distended with air during the first breath Figure , B. The entry of air into the alveoli improves oxygenation of the pulmonary vascular bed, further decreasing PVR.

    The increase in Q p raises left atrial pressures above right atrial pressures, closing the foramen ovale. SVR increases at birth, in part because of removal of the low resistance bed of the placenta.

    Lung disease: MedlinePlus Medical Encyclopedia

    As PVR becomes less than systemic, flow across the ductus reverses. Within the first 5 minutes after birth, oxygen-induced vasodilation and lung expansion decrease PVR to approximately half of systemic resistance. Over the first few hours after birth, the ductus arteriosus closes, largely in response to the increase in oxygen tension.

    At this point the normal postnatal circulatory pattern is established. The third stage of the transitional circulation occurs for 12 to 24 hours after birth and accounts for the greatest reduction in PVR. In the final phase of neonatal pulmonary vascular transition, further decline in PVR is accompanied by rapid structural remodeling of the entire pulmonary bed from the main pulmonary arteries to the capillaries. Maturation of smooth muscle function, thinning of endothelial cells Figure , C , and more gradual changes in elastic and connective tissue occur during the next few weeks.