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M W Aarnoudse

Publications and source records attributed to M W Aarnoudse.

7 recordsLinked to original sources
PubMed1984

Monocytes and radiation-induced atheromatosis in rabbits.

Previous experiments have shown that local irradiation of the carotid arteries of hypercholesterolemic rabbits results in the development of atheromatosis in the irradiated areas of the arteries. The process starts with the adherence of monocytes to the endothelial layer, their entrance into the subendothelial space, and their subsequent transformation into lipophages (foam cells). Prevention of this type of plaque formation can be achieved by prednisolone (in a lower concentration than previously used) (Vos et al. 1981) and by VP16-213 (Vepesid). Differential blood cell counts demonstrated that the animals subjected to treatment with prednisolone developed a moderate relative lymphocytopenia, whereas treatment with Vepesid resulted in a severe monocytopenia. Since prednisolone treatment only partially prevented plaque formation, whereas Vepesid seemed to fully inhibit the development of plaques, we conclude that although a role of the lymphocyte in the process of plaque formation cannot be excluded, the monocyte seems to play a crucial role in the pathogenesis of radiation-induced atheromatosis.

Animals↗
PubMed1983

On the cellular origin and development of atheromatous plaques. A light and electron microscopic study of combined X-ray and hypercholesterolemia-induced atheromatosis in the carotid artery of the rabbit.

The cellular origin and development of radiation-induced atheromatous plaques in the carotid artery of the hypercholesterolemic rabbit have been studied morphologically from a few hours post-irradiation up to several weeks later. As early as 8 h following local X-irradiation (500 or 1,000 rad) mononuclear cells, presumably blood monocytes, enter the subendothelial space. The cells have disappeared again 10 days post-irradiation in normocholesterolemic animals. In irradiated hypercholesterolemic animals, however, the invading mononuclear cells transform into lipophages and become so-called foam cells, visible from the second day post-irradiation. The number of lipophages increases with time resulting in plaques of about 5-10 cell layers after 20 days. From 20 days post-irradiation onwards smooth muscle cells enter the plaque by migrating from the tunica media through the fenestrations of the lamina elastica interna. Smooth muscle cells are found to contain less lipid vacuoles than monocyte-derived lipophages. At 30 days post-irradiation the smooth muscle cells have formed parallel layers in the luminal side of the plaque encapsulating an inner core of foam cells and other material. The morphology of the plaque at 30 days post-irradiation is similar to that reported for advanced plaques developing in rabbits by mere cholesterol feeding over a relatively long period. In irradiated normocholesterolemic and in non-irradiated hypercholesterolemic rabbits plaques are not observed in the carotid arteries during the experimental period. The early involvement of blood monocytes has been separated from the later role of medial smooth muscle cells in radiation-induced plaque formation. The results suggest that the underlying process in this lesion may be understood in terms of a sterile inflammation, complicated by an immediate fatty degeneration and followed by repair phenomena. The combination of hypercholesterolemia and ionizing radiation may serve as a useful experimental model for further studies in various animal species on why and how plaques originate, develop or regress and how they could possibly be prevented. The relevance of the results to radiotherapy in humans is mentioned briefly.

Animals↗
PubMed1978

Initial events in radiation-induced atheromatosis. II. Damage to intimal cells.

The carotid artery of the rabbit is a suitable blood vessel to study radiation induced atheromatosis in hypercholesteremic animals, because no plaque formation occurs within two months after the start of a 0.5% cholesterol diet. Cholesterol contents as high as 2% however, do give atheromatous plaques in the carotid artery without prior irradiation. As early as five hours after local irradiation of the carotid artery activation of the plasma membrane-bound enzyme alkaline phosphatase could be observed in some intimal cells. Two to three days after irradiation the activity disappeared. This phenomenon was observed in normo-and hypercholesteremic irradiated arteries. Depending on the lipid content of the blood, infiltration of lipids was observed at one day after the irradiation or later, accompanied by activation of beta-glucuronidase in the innermost layer of medial cells. Hereafter plaque formation started and cell proliferation could be found in the subendothelial space. It is assumed that because of the irradiation, the endothelial cells of the carotid artery are damaged in such a way that they do not function properly as a barrier against lipoprotein entrance from the blood into the arterial wall. The lipid infiltration caused lysosomal activation and probably cellular proliferation.

Alkaline Phosphatase↗
PubMed1977

Arterial wall damage by X-rays and fast neutrons.

Radiation-induced atheromatosis has been studied for 200 kVp X-rays and 15 MeV neutrons. From the results of two earlier experiments, a r.b.e. less than 1 was expected for neutrons. (1) Irradiation of blood-vessels causes depolymerization of the mucopolysaccharides in the vessel wall, resulting in atheromatosis, and (2) in two other mucopolysaccharide systems a r.b.e. less than 1 is observed for fast neutrons. Irradiation of the carotid arteries of a total number of 120 hypercholesterolaemic rabbits, divided over several groups, with 500 and 1000 rad of X-rays or neutrons results, however, in atheromatous plaques which are more pronounced for neutrons than for X-rays at the 500 rad dose-level; for a dose of 1000 rad the effect of neutrons is less extensive than the effect of X-rays. These results lead to the assumption that the origin of the atheromatosis seems not only to be the mucopolysaccharide depolymerization, but that radiation induced damage at the cellular level must be taken into account.

Animals↗