Radiation Damage and Subendothelial Repair to Rabbit Ear Chamber Microvasculature: An in Vivo and Histologic Study

Dimitrievich, George S.; Hausladen, Silke; Kuchnir, F.T.; Griem, Melvin L.

doi:10.2307/3574436

Cited by 35 publications

(5 citation statements)

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“…In contrast, a complete destruction of the capillary plexus and small feeding vessels has been observed in CAM12 exposed to 20 Gy SLR. Similar findings have been reported in numerous previous studies using other animal models (27)(28)(29)(30)(31).…”

Section: Discussionsupporting

confidence: 89%

Microbeam Radiation-Induced Tissue Damage Depends on the Stage of Vascular Maturation

Sabatasso

Laissue

Hlushchuk

et al. 2011

International Journal of Radiation Oncology*Biology*Physics

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Section: Discussionsupporting

confidence: 89%

Microbeam Radiation-Induced Tissue Damage Depends on the Stage of Vascular Maturation

Sabatasso

Laissue

Hlushchuk

et al. 2011

International Journal of Radiation Oncology*Biology*Physics

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“…In the heart and in irradiated tumor vasculature, findings support transcellular communication between tissue and blood after fractionated radiotherapy or a single dose of 10-13 Gy (52,53). Paracellular communication would seem to be more relevant at doses where overt killing of the endothelium is observed (54)(55)(56), and the resultant access to ECM in the context of dysfunctional endothelium could account for the accrual of von Willebrand factor by means of collagen binding domains of this platelet aggregating factor (57). Our findings suggest that lower doses where endothelial cells are not killed could still induce transient communication between the blood and myocardium.…”

Section: Discussionmentioning

confidence: 78%

Low-Dose Ionizing Radiation Stimulates Transcription and Production of Endothelin by Human Vein Endothelial Cells

et al. 2007

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“…The levels of radiation used herein may affect both the integrity of the microvasculature (27) and severely deplete the numbers of circulating platelets (28). It was therefore possible that the specific vascular damage caused by the MBP-reactive cells was accentuated by the absence of effective clotting mechanisms (no platelets), and by the presence of already irradiation-damaged microvasculature, the net result being the extravasation of erythrocytes into the parenchyma.…”

Section: Effect Of Injected Anti-cd4 Mab On Clinical and Histologicalmentioning

confidence: 99%

Experimental allergic encephalomyelitis in the absence of a classical delayed-type hypersensitivity reaction. Severe paralytic disease correlates with the presence of interleukin 2 receptor-positive cells infiltrating the central nervous system.

Sedgwick¹,

Brostoff²,

Mason³

1987

The Journal of Experimental Medicine

167

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One characteristic of experimental allergic encephalomyelitis (EAE) in all species is the presence of a considerable leukocyte infiltrate in the central nervous system (CNS). By adoptive transfer of EAE into irradiated or nonirradiated Lewis strain rats we now show that the bulk (greater than 90%) of infiltrating cells in the CNS are superfluous to the induction of disease, as lethally irradiated recipients, despite having very few infiltrating cells in the CNS, acquire severe paralytic EAE. The reduction in the level of infiltration in irradiated recipients is selective, however, as both irradiated and nonirradiated diseased animals have very similar numbers of cells expressing IL-2-R. Disease in irradiated recipient animals is associated with substantial submeningeal hemorrhage in the spinal cord and brain stem and similar hemorrhages are found in recipients rendered leukopenic with cytotoxic drugs. Clinical signs of disease and hemorrhage are preventable, however, by administration to the recipient rats of mAbs specific for the CD4 antigen. Classic delayed-type hypersensitivity (DTH) reactions are transferable with the same cells that produce EAE in both irradiated and nonirradiated recipient rats, but such transfer of DTH is observed only in nonirradiated recipient animals and not in irradiated rats. Collectively, the findings reported herein support the conclusion that the paralysis characteristic of acute EAE is mediated by the direct action of very small numbers of activated CD4+ lymphocytes that infiltrate the CNS and produce their effects by inducing vascular damage. The findings are not consistent with reports that the lesions in EAE are produced by a classic DTH reaction.

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Radiation Damage and Subendothelial Repair to Rabbit Ear Chamber Microvasculature: An in Vivo and Histologic Study

Cited by 35 publications

References 0 publications

Microbeam Radiation-Induced Tissue Damage Depends on the Stage of Vascular Maturation

Microbeam Radiation-Induced Tissue Damage Depends on the Stage of Vascular Maturation

Low-Dose Ionizing Radiation Stimulates Transcription and Production of Endothelin by Human Vein Endothelial Cells

Experimental allergic encephalomyelitis in the absence of a classical delayed-type hypersensitivity reaction. Severe paralytic disease correlates with the presence of interleukin 2 receptor-positive cells infiltrating the central nervous system.

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