Mechanisms of Acute Injury in the Gamma-Irradiated Chicken: Effects of a Protracted or a Split-Dose Exposure on the Fine Structure of the Microvasculature

Stearner, S.P.; Sanderson, Margaret H.

doi:10.2307/3573271

Cited by 24 publications

(12 citation statements)

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“…This was contradicted by Withers et al (1980) and discussion has continued until now (Graham et al 1990;Jain 1988;Msirikale et al 1987;Rose et al 1999;Waters et al 1996), though as yet without any input in the form of ultrastructural tracer data. The resulting acute episode of vascular hyperpermeability results from endothelial cell lysis or opening of intercellular junctions (Stearner and Sanderson 1972). The resulting acute episode of vascular hyperpermeability results from endothelial cell lysis or opening of intercellular junctions (Stearner and Sanderson 1972).…”

Section: Introductionmentioning

confidence: 99%

“…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%

“…Tracer studies, if they visualised the vessel wall structure at all, were restricted to light microscopy (see, for example, Cohen et al 1994;Siegal et al 1996). Only three studies localised a tracer ultrastructurally in hyperpermeable vessel walls (colloidal carbon: Dvorak et al 1988;Stearner and Sanderson 1972;macromolecules: Feng et al 1999). Only three studies localised a tracer ultrastructurally in hyperpermeable vessel walls (colloidal carbon: Dvorak et al 1988;Stearner and Sanderson 1972;macromolecules: Feng et al 1999).…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…The sparing effect of dose fractionation (SDF) has been demonstrated in a number of organisms involving cell killing, microvasculature damage and pupariation delay as parameters [1,5,9,10,19,21 ]. When given as postirradiation treatment after single exposure, caffeine increases the delay in a synergistic manner.…”

mentioning

confidence: 99%

“…The sparing effect of dose fractionation (SDF) has been demonstrated in a number of organisms involving cell killing, microvasculature damage and pupariation delay as parameters [1,5,9,10,19,21 ]. The sparing effect of dose fractionation (SDF) has been demonstrated in a number of organisms involving cell killing, microvasculature damage and pupariation delay as parameters [1,5,9,10,19,21 ].…”

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confidence: 99%

Influence of caffeine on sparing effect of dose fractionation in housefly larvae

Srinivasan

Kesavan

1979

Radiat Environ Biophys

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Caffeine, given during interfraction interval, abolishes the sparing effect of dose fractionation observed for delay of pupariation in Musca domestica larvae. When given as postirradiation treatment after single exposure, caffeine increases the delay in the synergistic manner. Pretreatment of the larvae with ascorbic acid for 3 h protects from radiation-induced delay whereas pretreatment with caffeine does not have any effect. Combination of ascorbic acid and caffeine pretreatment protects the larvae only at low concentration (0.05%) and not at high concentration (0.1%).

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Biological characterization of a high energy neutron beam for radiation therapy

Montour

Wilson

Rogers

et al. 1974

Cancer

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In anticipation of the use of the Naval Research Laboratory (NRL) 35‐MeV neutron facility for radiotherapy by the Middle Atlantic Neutron Therapy Association (MANTA), RBE values were obtained for a diversity of biological end points. Animals were exposed to neutrons at a dose‐rate of approximately 60 rads/min, in Lucite exposure chambers which also served as scattering material. Parallel experiments were performed, using the same exposure apparatus, in which animals were exposed to 60Co gamma rays given at approximately 100 rads/min. RBE values were found as follows: mouse LD50/5 1.68; mouse LD50/30 1.80; mouse endogenous spleen colonies, 1.58; mouse thymic involution (ED50) 1.45; mouse splenic involution (ED50), 1.40; chick LD50/30 hour 1.81.

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Mechanisms of Acute Injury in the Gamma-Irradiated Chicken: Effects of a Protracted or a Split-Dose Exposure on the Fine Structure of the Microvasculature

Cited by 24 publications

References 0 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

Influence of caffeine on sparing effect of dose fractionation in housefly larvae

Biological characterization of a high energy neutron beam for radiation therapy

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