Early Effects of Beta Irradiation on Dermal Vascular Permeability to Plasma Proteins

Song, Chang W.; Anderson, Robert S.; Tabachnick, Joseph

doi:10.2307/3571844

Cited by 36 publications

(19 citation statements)

References 21 publications

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“…It has been postulated that radiation damages the integrity of the microvascular endothelium, thereby inducing transvascular hyperpermeability to plasma proteins, with subsequent fibrin deposition in the extravascular spaces. The newly deposited fibrin is eventually replaced by collagen fibers, resulting in fibrosis and parenchymal cell atrophy, which are characteristic of the late phase of radiation-induced injuries in normal tissues (1– 3). …”

Section: Introductionmentioning

confidence: 99%

“…Numerous studies have demonstrated an increase in macromolecular extravasation after irradiation in various normal tissues (1–16), as well as in tumors (17). These previous studies have mostly determined the total amount of extravasated macromolecules that result from an increase in the permeability surface area product (defined by the vascular permeability and vascular surface area); however, vascular permeability itself has not yet been measured directly.…”

Section: Introductionmentioning

confidence: 99%

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Mast Cells Contribute to Radiation-Induced Vascular Hyperpermeability

et al. 2016

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Induction of vascular hyperpermeability is one of the early vascular responses to radiation exposure and is considered to contribute to subsequent fibrosis and tissue injuries. However, the mechanism underlying radiation-induced hyperpermeability has not yet been clearly elucidated. Here, we provide experimental evidence indicating that mast cells contribute to the increase in vascular permeability for albumin in normal mouse skin after irradiation. Vascular permeability in the skin of C3H mice increased after 2, 15 and 50 Gy irradiation, peaked at 24 h after irradiation and gradually decreased thereafter to the baseline level within 3–10 days. Both the extent and duration of hyperpermeability were dose dependent. We found significant degranulation of mast cells in the skin after 15 Gy irradiation. To further investigate the role of mast cells in the radiation-induced increase in vascular permeability, we measured vascular permeability in the skin of mast cell-deficient mice (WWv) and their wild-type littermates at 24 h after irradiation. Vascular permeability in WWv mice did not change, whereas that in wild-type mice significantly increased after irradiation. There were no appreciable changes in the total tissue levels of vascular endothelial growth factor or endothelial nitric oxide synthase after 15 Gy irradiation and there was no detectable expression of inducible nitric oxide synthase. Collectively, these results show that exposure to radiation induces vascular hyperpermeability in a dose-dependent manner and that mast cells contribute to this process.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mast Cells Contribute to Radiation-Induced Vascular Hyperpermeability

et al. 2016

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“…We shall argue that the third is (1) The tumour vasculature reacts to radiation quickly (relative to that of normal tissues) by active vasodilation. This would increase the size of the "inert reservoir " so that, after Nembutal it would be able to accept more of the blood shunted away from other organs (it should be noted that increased vascular permeability, such as reported by Song et al (1966) and Jolles and Harrison (1966) Song et al (1966) found that Indomethacin could prevent the radiation-induced increase in vascular permeability in the dermis and epidermis of cats. Indomethacin is one of the most powerful inhibitors of prostaglandin synthesis (Williams and Morley, 1973;Vane, 1971) and these hormones, which have been implicated in the local control of the circulation, have been shown to be produced locally, following various types of stimuli such as trauma, anoxia and various types of cellular injury (StaszewskaBarezak and Vane, 1975).…”

Section: Discussionmentioning

confidence: 99%

“…It is known that, following irradiation, the vasculature of normal tissues undergoes functional changes (Song, Anderson and Tabachnick, 1966;Reinhold, et al, 1974), such as increased permeability, which can be prevented to some extent by anti-inflammatory drugs such as Indomethacin (a potent inhibitor of prostaglandin synthesis). What is not known, among other things, is (1) whether the tumour vascular bed is also sensitive to the effects of any vasoactive substances which may be released by radiation-killed cells and (2) whether radiation-induced functional vascular damage follows the same time course in tumours and normal tissues.…”

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confidence: 99%

Effects of X-rays on vascular function in transplanted tumours and normal tissues in the mouse

Zanelli¹,

Lucas²

1976

Br J Cancer

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Summary.-The effects of X-radiation on the Nembutal-induced redistribution of the cardiac output in two types of transplanted mouse tumours and some normal mouse tissues have been investigated, using rubidium-86 and 125I-human serum albumin. Irradiation causes an increase in 86Rb uptake (relative blood perfusion) by the tumours of anaesthetized mice, but has little or no effect in non-anaesthetized mice. The increase is dose-and time-dependent. Tumour plasma space is not significantly affected by radiation and Nembutal. Muscle blood perfusion is severely decreased in anaesthetized mice and is not affected by radiation, at least within the time limits of the experiments. This means that radiation-induced functional vascular changes in normal and neoplastic tissues follow different time courses. On the basis of the present results, and of the results of other authors, it is argued that irradiation damages the vasculature of tumours in such a way that it becomes more sensitive to changes in systemic blood pressure.

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“…The increase in the water content of irradiated tissues [11][12][13] is an other factor which could account, by itself, or in association with the above-mentioned changes, for the matrix modifications.…”

Section: Discussionmentioning

confidence: 99%

Acute Ultrastructural Alterations in Irradiated Proliferative Chondrocytes of Rat Growth Cartilage

Klein‐Szanto¹,

Cabrini²

1974

Pathobiology

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Ultrastructural changes in proliferative chondrocytes of rats exposed to 7 krads of were studied X-rays 2, 4, 8, and 10 days after irradiation. The lesion is characterized by disorganization of the epiphyseal plate with marked involutive changes of the cells. Two days after irradiation, there is a slight dilation of the endoplasmic reticulum. As from the fourth post irradiation day on, a marked saccular and lacunar dilation of these structures could be seen. Vacuolar structures related with the Golgi complex and lipid droplets could be noted 4, 8, and 10 days after irradiation. Lysosomes, which normally are not seen in proliferative chondrocytes, were also noted during this study. Cytoplasmic fragmentation and an increasing number of calcifying globules could be observed in the 8- and 10-day groups. Nuclear fragmentation, lobulation, and the presence of binucleated viable cells were other signs of cell division alteration produced by radiation. The decrease of proteoglycan granules and collagen fibrils in association with the endoplasmic reticulum and Golgi changes points to a probable damage of the synthetic and secretory activities of chondrocytes.

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Early Effects of Beta Irradiation on Dermal Vascular Permeability to Plasma Proteins

Cited by 36 publications

References 21 publications

Mast Cells Contribute to Radiation-Induced Vascular Hyperpermeability

Mast Cells Contribute to Radiation-Induced Vascular Hyperpermeability

Effects of X-rays on vascular function in transplanted tumours and normal tissues in the mouse

Acute Ultrastructural Alterations in Irradiated Proliferative Chondrocytes of Rat Growth Cartilage

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