Mechanisms of Resistance and Reversal in the Initial Radiation Response in the Chick

Stearner, S.P.; Tyler, Sylvanus A.; Sanderson, Margaret H.; Christian, E.J.B.

doi:10.2307/3571014

Cited by 11 publications

(2 citation statements)

References 13 publications

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“…The resulting acute episode of vascular hyperpermeability results from endothelial cell lysis or opening of intercellular junctions (Stearner and Sanderson 1972). In such "fractionated" protocols, repair processes can occur, microvessel integrity can be preserved (Rubin and Casarett 1966) and the tissues tolerate sequential small doses much better than a single large dose (Stearner and Sanderson 1972;Stearner et al 1961). This damage leaves physical gaps in the microvessel wall, permitting passive fluxes into the extravascular compartment.…”

Section: Introductionmentioning

confidence: 99%

Vascular permeability and hyperpermeability in a murine adenocarcinoma after fractionated radiotherapy: an ultrastructural tracer study

Debbage

Kreczy

et al. 2000

Histochem Cell Biol

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Large radiation doses cause postradiation vascular hyperpermeability by disrupting endothelia. The cumulative sequences of small doses (fractionated radiotherapy) standard in clinical practice cause it too, but not by endothelial disruption: the mechanisms are unknown. In this study, correlated fluorescent and ultrastructural localisation of a tracer revealed the architecture, fine structure and function of microvessels in mouse AT17 tumours, before and after 42 Gy fractionated radiation. Before irradiation, tumour vascular permeability lay in the normophysiological range defined by the gut and cerebral cortex. A double barrier regulated permeability: vesicular transport through the endothelial wall required approximately 2 h and then the basement membrane charge barrier trapped tracer for 2 h longer. Irradiation abolished the double barrier: tracer passed instantly through both endothelial wall and underlying basement membrane, forming diffusion haloes around microvessels within 2-5 min. Structurally, irradiated tumour microvessels were lined by a continuous and vital endothelium with closed interendothelial junctions; endothelial basement membranes were intact, though loosened. Irradiated endothelia exhibited extremely active membrane motility and intracellular vesicle trafficking. Radiation treatment raised vascular permeability by enhancing transendothelial transcytosis, and by altering the passive filter properties of the subendothelial basement membrane. This type of vascular hyperpermeability should be susceptible to pharmacological modulation.

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Section: Introductionmentioning

confidence: 99%

Vascular permeability and hyperpermeability in a murine adenocarcinoma after fractionated radiotherapy: an ultrastructural tracer study

Debbage

Kreczy

et al. 2000

Histochem Cell Biol

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“…A similar linear decay of radiation damage, as also postulated in model A of Brown et al (1960), had been suggested earlier as occurring in chicks for deaths at earlier times (Steamrner and Tyler 1957). The 0-2 day deaths of the chick are biologically quite different from the bone-marrow deaths of the mouse and further work (Stearner, Tyler, Sanderson and Christian 1961) suggests that the chick can be made positively radioresistant by a previous exposure to radiation, a phenomenon which has never been described in the mouse. Nevertheless the observations that there is a linear decay of radiation damage over a period of some hours in organisms as different as the mouse, the 3-4 day old chick, and the chick embryo (Tyler and Steamrner 1960) suggest that there is here a general radiobiological phenomenon.…”

Section: Discussionmentioning

confidence: 93%

The Effect of Dose-rate and Fractionation on Acute Mortality in X-irradiated Mice. Part II

Brown

Corp

Mole

1962

International Journal of Radiation Biology and Related Studies

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1. Changing the exposure time from 15 min to less than 1 min and the dose-rate from 54 to 1100 rads/min did not reduce the LD 50 1 / 0 by more than a few per cent. Changes in the uniformity of tissue dose, as by changing the direction of the x-ray beam, were quantitatively much more important.2. The effect of increasing exposure time from 6 to 36 hours with continuous irradiation was compared with other exposures spread over similar periods of time but divided into 2, 4 or 18 equal fractions, each at a relatively high dose-rate. Neither with continuous nor with fractionated exposures did the LD 50 /30 increase indefinitely as overall exposure time was prolonged. The rapid phase of decay of radiation damage appeared to stop early, at 6 hours, after a single dose but not until after 18 hours of prolonged exposure.

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Protection against early radiation injury to the microvasculature

Stearner

Christian

1970

Microvascular Research

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Mechanisms of Resistance and Reversal in the Initial Radiation Response in the Chick

Cited by 11 publications

References 13 publications

Vascular permeability and hyperpermeability in a murine adenocarcinoma after fractionated radiotherapy: an ultrastructural tracer study

Vascular permeability and hyperpermeability in a murine adenocarcinoma after fractionated radiotherapy: an ultrastructural tracer study

The Effect of Dose-rate and Fractionation on Acute Mortality in X-irradiated Mice. Part II

Protection against early radiation injury to the microvasculature

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