Chest
Special ReportStructure and Function in Pulmonary Hypertension: New Perceptions
Section snippets
HYPOXIA
Hypoxia is an important clinical cause of pulmonary hypertension, as seen in chronic bronchitis,4, 5, 6 in the hypoxic hypertension associated with altitude, and with hypoventilation associated with sleep disorders. The adult chronic bronchitis patient is more likely to develop polycythemia than the child or adolescent with cystic fibrosis,7 in whom polycythemia is rare. In the adult, the airway obstruction of severe panacinar emphysema, although associated with a major reduction of vascular
MONOCROTALINE
Monocrotaline, a toxic alkaloid, produces pulmonary hypertension with increased muscularity similar to hypoxia, but differences also are present between the two models. Monocrotaline produces an endothelial injury causing obliterative lesions in microvessels.21 The pressure rise in animals exposed to monocrotaline correlates closely with obliteration of the small arteries, not with the extension of muscle as in hypoxia.22 While after monocrotaline new muscle is apparent by light microscopy at
OXYGEN TOXICITY
Pulmonary hypertension is caused also by high oxygen; it is an expression of oxygen toxicity (Fig 8). In the rat, levels above 90 percent are rapidly fatal, whereas 87 percent O2 allows survival after acute injury so that adaptation can be analyzed.24, 25 After as short a period as seven days, there is a 50 percent rise in pulmonary artery pressure and a doubling of resistance. While injury of oxygen toxicity is important, the effect of return to air is intriguing (Fig 9). There are two related
PRIMARY OR IDIOPATHIC PULMONARY HYPERTENSION
In the category idiopathic pulmonary hypertension, included are both the arterial26 and venous varieties, emphasizing that the obstructive vascular lesions can be mainly at one or other of these sites. It also underlines that the diagnosis of idiopathic pulmonary arterial hypertension immediately puts the clinician on enquiry to exclude that it is not the presenting sign of pulmonary venous hypertension.27 At Children’s Hospital, we have been impressed in the last few years with the high
PULMONARY HYPERTENSION OF THE NEWBORN
The smallest arteries of the fetal circulation are relatively the most muscular; arteries of all sizes have a relatively thicker wall in the fetus and newborn than in the adult, supporting the adage that the fetal circulation is more muscular than in the adult (Fig 11).28, 29 But whereas in the adult muscular arteries are found in alveolar walls, that is within the acinus, in the normal fetus and newborn, virtually none of the alveolar wall arteries are fully muscularized. In this respect, the
STRUCTURAL FEATURES OF PRECAPILLARY UNIT
Toward the end of each pulmonary arterial pathway, the complete muscle coat gives way to a segment where muscle discontinues before it disappears as judged by light microscopy, from arteries still larger than capillaries (Fig 3).29 Thus, muscular, partially muscular, and nonmuscular arteries can be identified making up a precapillary segment; a similar segment is present in the postcapillary or venous segment. By electron microscopy, in the nonmuscular part of the wall, two types of precursor
REACTIVITY
The nature of reactivity of the pulmonary circulation perhaps holds as many mysteries as it did at the time of Simon Rodbard. The behavior of the pulmonary circulation to a given stimulus depends more on its recent history than on the stimulus used. It is not perhaps surprising then that there are drugs whose action in air flip flops to the opposite under hypoxia. Does this point to different metabolic behavior, to change in receptors or literally to change in structure? The precursor cells
IN VITRO STUDY OF ARTERIAL REACTIVITY IN SMALL RESISTANCE ARTERIES IN PRECAPILLARY ALVEOLAR UNIT
Probably the resistance arteries represent the smallest ones to which myography can be applied.43 We have developed a technique whereby we can look in vitro at the reactivity of blood vessels using slices of tissue.44, 45 After a short time in culture medium (we commonly use 15 minutes), tissue is rapidly fixed in glutaraldehyde. The elastic laminae are traced and can be used to identify the degree of “constriction” (or retraction) of the arteries in culture. Using a digitizer, microscopic
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2023, Journal of Biological ChemistryThe Relationship Between the Right Ventricle and its Load in Pulmonary Hypertension
2017, Journal of the American College of CardiologyCitation Excerpt :Arterial and venous data in health and PH reported by Chazova et al. (5) suggest that changes in the veins may indeed contribute to PVR. Reid (6) has suggested that rarefaction may also play a role. Further research in this area is required to understand the structural basis of increased resistance in the pulmonary vascular bed.
Regional Circulation
2011, Pediatric Critical Care: Expert Consult Premium EditionDiseases of Pulmonary Circulation
2011, Pediatric Critical Care: Expert Consult Premium Edition
This paper was the 7th Simon Rodbard Memorial Lecture presented at the 50th Anniversary Meeting of the American College of Chest Physicians, Dallas, Oct 10, 1984.