Biomedical subjects

N Wagenvoort

Publications and source records attributed to N Wagenvoort.

At least 19 recordsLinked to original sources

PubMed1993

Pulmonary vasoconstriction in oleic acid induced lung injury. A morphometric study.

Distribution and severity of active vasoconstriction of muscular pulmonary arteries were morphometrically assessed in anaesthetized, paralysed and mechanically ventilated pigs with respiratory distress, induced by oleic acid. Vasoconstriction was deduced from the medial thickness which was measured and expressed as a percentage of external diameter. Six pigs received oleic acid (0.12 +/- 0.07 ml/kg), dissolved 1:1 in 96% alcohol, in multiple injections of 0.1 ml. Six pigs were used as controls. After the oleic acid injections a stable hypoxaemia (PaO2 = 57 +/- 8 mmHg, at an inspiratory oxygen fraction of 0.6) and pulmonary hypertension (mean Ppa = 36 +/- 2 mmHg) were obtained for several hours. Electron microscopy revealed swelling of endothelial cells with signs of degeneration. Medial thickness was far greater in the oleic acid group than in the control group; overall mean values were 8.1 +/- 3.2 and 3.8 +/- 1.7% respectively (P < 0.001). Arteries with prominent vasoconstriction were lying in clusters. This pattern was the same in dependent and non-dependent regions. We concluded that in oleic acid induced respiratory distress active vasoconstriction of muscular pulmonary arteries is an important factor in the development of pulmonary hypertension. Besides vasoconstriction, endothelial swelling and intravascular clotting may contribute to the development of pulmonary hypertension.

Animals↗

PubMed1985

Pulmonary veno-occlusive disease: involvement of pulmonary arteries and review of the literature.

Pulmonary vessels from 26 patients with pulmonary veno-occlusive disease were studied histologically and morphometrically. In addition to the well-known obstruction of veins and venules, pulmonary arteries were also narrowed or obliterated in approximately half of the patients. It is unlikely that the arterial intimal fibrosis, which was sometimes as severe as the fibrosis in the veins, was secondary to the venous obstruction; rather, like the venous alterations, it probably resulted from organization of thrombi. It is possible that primary damage to the vascular wall elicited thrombosis. Such an injury may also have caused the arterialization of the venous walls, a common finding that cannot always be explained by distal narrowing of larger veins. Although the etiology of pulmonary veno-occlusive disease is obscure, it seems increasingly likely that multiple noxious agents may induce this condition. In children no predilection for either sex has been observed, but in adults, men are affected twice as often as women.

Adolescent↗

PubMed1984

Longitudinal smooth muscle in pulmonary arteries. Occurrence in congenital heart disease.

In lung biopsy specimens of 19 patients with congenital heart disease and pulmonary hypertension, in addition to the common features of plexogenic arteriopathy, longitudinal smooth muscle cells were found in small pulmonary arteries. These cells were arranged in bundles or layers, particularly in the intima but sometimes within the media or adventitia of the arteries. They often caused severe narrowing of the lumen. Corrective surgery of the cardiac defect was performed in 14 patients. The results suggested that even when these changes are wide-spread and severe, they do not stand in the way of a favourable post-operative course. In one patient who underwent a banding procedure of the pulmonary artery, virtually complete regression of the smooth muscle layers could be demonstrated in a second biopsy, taken 5 years later during a corrective operation.

Adolescent↗

PubMed1984

Reversibility of plexogenic pulmonary arteriopathy following banding of the pulmonary artery.

In 28 patients with congenital heart disease with a shunt and pulmonary hypertension, lung biopsy specimens were taken during a banding procedure of the pulmonary artery; then, in the same patients, lung tissue became available during correction of the cardiac defect some years later. In this way the regression of pulmonary vascular changes could be studied. Medial hypertrophy appeared to have a prominent tendency to regression. With intimal lesions, regression depended to a large extent on the type of lesion. Intimal thickening based on longitudinal smooth muscle tissue was almost completely reversible. Post-thrombotic intimal fibrosis was also potentially reversible. In plexogenic pulmonary arteriopathy, the earlier lesions, particularly cellular intimal proliferation, showed regression. Concentric-laminar intimal fibrosis regressed as long as it was mild, that is, occluding less than one fifth of the average arterial lumen. If more severe, there was no tendency to regression and often it even progressed. Changes like fibrinoid necrosis and plexiform lesions are ominous because of their tendency to progression. Since preoperative open lung biopsies now are often undertaken for evaluation of hypertensive pulmonary vascular disease, when corrective operability is dubious, these findings may serve as a guide in reporting on such biopsy specimens.

Adolescent↗

PubMed1983

The density of muscularized pulmonary arteries in normal lungs: a morphometric study.

In a series of 24 subjects who ranged in age from 2.5 months to 50 years and who were not suffering from cardiac or pulmonary disease, the density of muscularized pulmonary arteries was established in relation to their diameter. The number of arteries per unit area of lung tissue was corrected to account for various states of lung expansion of or collapse. The density of pulmonary arteries decreased rapidly during the first few years of life, then more gradually during the first two decades of life. Concomitantly, the diameter of the smallest muscularized arterial branches increased with age. These findings indicate that, even after completed development of lung tissue, there is a retraction of media in the sense that small arterioles lose their media, a process that continues until early adulthood. The values thus obtained may serve as a standard for comparison when the pulmonary arterial density is studied in cases of pulmonary hypertension in which it reportedly is greatly diminished.

Adolescent↗

PubMed1982

Pulmonary veins in high-altitude residents: a morphometric study.

The thickness of the media of pulmonary veins and arteries was morphometrically assessed in 12 normal adults resident at altitudes over 3000 m and 12 resident at sea level. The pulmonary veins in the latter group were very thin walled. The average thickness of the pulmonary venous media in the group of highlanders was significantly thicker but this appeared to be due to prominent medial hypertrophy in seven individuals, five others having normal or near-normal pulmonary veins. In six of the 12 highlanders bundles of longitudinal smooth muscle cells occurred in the venous intima. There was close correlation between the thickness of the venous and that of the arterial media, suggesting an individual reactivity with a simultaneous response of all pulmonary vascular smooth muscle to high-altitude hypoxia. Hypertrophy of the media of pulmonary veins is likely to be an expression of venoconstriction and narrowing of the venous lumen may be enhanced by the development of longitudinal smooth muscle cells in the intima. Possibly venoconstriction is one of the factors responsible for high-altitude pulmonary oedema.

Adult↗

PubMed1982

Smooth muscle content of pulmonary arterial media in pulmonary venous hypertension compared with other forms of pulmonary hypertension.

The number of smooth muscle cells per unit of surface area of the media of muscular pulmonary arteries was assessed and expressed as an index of medial smooth muscle density. The relative medial thickness of these arteries was also established. Subjects were ten children and ten adults in each of the following conditions: normal, congenital cardial defects with a left-to-right shunt (CCD), primary pulmonary hypertension (PPH), and mitral stenosis (MS); ie, 80 persons in all. The density of medial smooth muscle is generally the same in normal control subjects and in patients with CCD or PPH and is independent of the medial thickness. The index is also the same in children with MS, but significantly reduced in adult patients with MS, apparently by a prominent contribution of collagen and edematous ground substance to the structure of the media. This may explain, at least to some extent, the discrepancy often observed in adult patients with MS, of a very thick media associated with mild elevation of pulmonary arterial pressure. The present study leaves open the possibility that other factors, decisive for this elevation of pressure, are involved. The differences in medial structure may also account for some hemodynamic differences between adults and children with MS.

Adolescent↗

PubMed1976

Pulmonary venous changes in chronic hypoxia.

Lung tissue from 14 normal residents of high altitude regions, 10 patients with chronic bronchitis and emphysema, and 1 patient with Pickwickian syndrome was studied with regard to the occurrence of pulmonary vascular changes. In addition to the well-known pulmonary arterial alterations, lesions in small pulmonary veins were found in the great majority of the cases. These changes, consisting of medial hypertrophy and arterialization and of bundles of smooth muscle cells within the venous intima, have not been described before in man. These findings suggest that alveolar hypoxia acts not only on small pulmonary arteries and arterioles but also on veins of small caliber, probably by inducing venoconstriction.

Adolescent↗

PubMed1974