Reoxygenation of tumours in “sandwich” chambers

Reinhold, H; Blachiewicz, B.; Berg-Blok, A. Van Den

doi:10.1016/0014-2964(79)90083-5

Cited by 35 publications

(12 citation statements)

References 20 publications

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“…However, there is evidence for rapid fluctuations in blood flow in individual blood vessels within tumors, which could produce transient hypoxia persisting for only seconds or minutes [5,[73][74][75][76]. If tumor cells are hypoxic for periods of time shorter than the irradiation time, they will not be measured as fully resistant.…”

Section: Assumptions Made In All Hypoxic Fraction Assay Techniquesmentioning

confidence: 99%

“…Reinhold et al [74,75] found fluctuations in blood flow through individual tumor blood vessels which could lead to transient perfusion deficits lasting seconds to minutes. Sutherland [76] and Brown [5] suggest that such blood flow fluctuations could produce transient hypoxia in areas of tumor which appear to have adequate vasculature.…”

Section: Chronic Versus Transient Hypoxiamentioning

confidence: 99%

“…Moreover, the duration of post-irradiation hypoxia in vivo is unknown. As there is evidence in some tumors for rapid changes in blood flow and oxygenation after irradiation [74,75,130,[185][186][187][188], and for transiently hypoxic cells [5,76], it is unclear whether hypoxic cells remaining in situ after treatment remain severely hypoxic or whether they become aerobic soon enough to influence repair processes.…”

Section: Effects Of Hypoxia On Cellular Radiosensitivity and Repairmentioning

confidence: 99%

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Tumor hypoxia: its impact on cancer therapy

1987

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The presence of radiation resistant cells in solid human tumors is believed to be a major reason why radiotherapy fails to eradicate some such neoplasms. The presence of unperfused regions containing hypoxic cells may also contribute to resistance to some chemotherapeutic agents. This paper reviews the evidence that radiation resistant hypoxic cells exist in solid tumors, the assumptions and results of the methods used to detect hypoxic cells, and the causes and nature of tumor hypoxia. Evidence that radiation resistant hypoxic cells exist in the vast majority of transplanted rodent tumors and xenografted human tumors is direct and convincing, but problems with the current methodology make quantitative statements about the magnitude of the hypoxic fractions problematic. Evidence that radiation resistant hypoxic cells exist in human tumors is considerably more indirect than the evidence for their existence in transplanted tumors, but it is convincing. However, evidence that hypoxic cells are a significant cause of local failure after optimal clinical radiotherapy or chemotherapy regimens is limited and less definitive. The nature and causes of tumor hypoxia are not definitively known. In particular, it is not certain whether hypoxia is a chronic or a transient state, whether hypoxic cells are proliferating or quiescent, or whether hypoxic cells have the same repair capacity as aerobic cells. A number of new methods for assessing hypoxia are reviewed. While there are still problems with all of the new techniques, some of them have the potential of allowing the assessment of hypoxia in individual human tumors.

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Section: Assumptions Made In All Hypoxic Fraction Assay Techniquesmentioning

confidence: 99%

Section: Chronic Versus Transient Hypoxiamentioning

confidence: 99%

Section: Effects Of Hypoxia On Cellular Radiosensitivity and Repairmentioning

confidence: 99%

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Tumor hypoxia: its impact on cancer therapy

1987

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“…Thus, methods of quantifying angiogenesis and its inhibition have been developed, and in vivo and in vitro techniques are available for research on the different steps of angiogenesis, i.e. migration, pro liferation, differentiation and regression of endothelial cells [1], In vivo, methods of the analysis of angiogenesis in clude the rabbit ear chamber [2][3][4], the rat air pouch [5], the hamster cheek pouch [6,7], the chick embryo cho rioallantoic membrane (CAM) [8], the chick yolk sac [9,10] and the rabbit or rat cornea [11,12] assays. These models enable a direct observation of newly growing ves sels.…”

mentioning

confidence: 99%

New Model for the Study of Angiogenesis and Antiangiogenesis in the Chick Embryo Chorioallantoic Membrane: The Gelatin Sponge/ Chorioallantoic Membrane Assay

et al. 1997

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Several methods for the in vivo study of angiogenesis are available, and each angiogenic assay presents distinct advantages and disadvantages. In this study, we present a new method for the quantitation of angiogenesis and antiangiogenesis in the chick embryo chorioallantoic membrane (CAM), based on the implantation of gelatin sponges on the top of growing CAM, on day 8 of incubation. After implantation, the sponges were treated with a stimulator (recombinant human basic fibroblast growth factor, FGF2) or an inhibitor (a rabbit polyclonal anti-FGF2 antibody) of blood vessel formation. Blood vessels growing vertically into the sponge and at the boundary between sponge and surrounding CAM mesenchyme were counted by a morphometric method on day 12. In addition, to assess whether the gelatin sponge is an appropriate vehicle to deliver cultured cells and evaluate their angiogenic potential, mouse aortic endothelial cells were cotransfected with human FGF2 and the Escherichia coli β -galactosidase (β -GAL) reporter gene. Stable transfectants were absorbed by the sponge, and evaluation of the angiogenic response was paralleled by β -GAL staining to visualize implanted cells. This technique may facilitate the discovery and development of agonists or antagonists of angiogenesis.

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“…Using an eluent of 93% methanol and 7% phosphate buffer (pH 7, 10 mM), the bacteriochlorophyll a yielded a single blue spot (relative mobility approximately 0.5) on Machery-Nagel Nano-Sil C,8-100 TLC plates (Diiren, Germany). Bacteriochlorophyllin a was obtained by saponifying bacteriochlorophyll a as described by Oster et al (1964) (Reinhold et al, 1979) Photodynamic therapy Light of 760 nm wavelength was obtained from a dye laser (Spectra Physics 375B, with Styryl 8), pumped by an argonion (Spectra Physics 171) laser. Light, at a power density of 100 mW/cm 2, was delivered to the chamber via an optical fibre and a lens system with diaphragm yielding a uniform beam of 10 mm diameter covering the entire window of the chamber (9 mm in diameter).…”

Section: Methodsmentioning

confidence: 99%

Fluorescence and photodynamic effects of bacteriochlorin a observed in vivo in 'sandwich' observation chambers

Leengoed

Schuitmaker²,

Veen³

et al. 1993

Br J Cancer

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Bacteriochlorin a (BCA), a derivative of bacteriochlorphyll a, is an effective photosensitiser in vitro and in vivo. BCA has a major absorption peak at 760 nm where tissue penetration is optimal. This property, together with rapid tissue clearance promises minor skin photosensitivity. The tissue localising and photodynamic properties of BCA were studied using isogeneic RMA mammary tumours, transplanted into subcutaneous tissue in transparent 'sandwich' observation chambers on the back of WAG/Rij rats. The fluorescence kinetics following an i.v. administration of 20 mg kg-1 BCA was assessed in blood vessels, tumour and normal tissue. Subsequently, the development of vascular- and tissue damage after a therapeutic light dose (760 nm, 600 J cm-2) was observed. Fifteen minutes post injection (p.i.), the fluorescence of BCA in the tumour reached a plateau value of 2.5 times the fluorescence in the normal tissue. From 1 h post injection the tumour fluorescence diminished gradually; after 24 h, the tumour fluorescence signal did not exceed that of the normal tissue. Following photodynamic therapy (PDT), 24 h p.i., complete vascular stasis was observed 2 h post treatment in the tumour only, with subsequent recovery. The presence of viable tumour cells following PDT was assessed by histology and re-transplantation of treated tumour tissue from the chamber into the flank immediately or 7 days after treatment. In both cases tumour regrowth was observed. BCA-PDT (20 mg kg-1, 760 nm, 100 J cm-2) 1 h after BCA administration, an interval which gives the optimal differential between tumour and normal tissue, was sufficient to prevent tumour regrowth. However, this only occurred when re-transplantation was performed 7 days after PDT. During PDT, 1 h p.i., vascular damage in tumour and normal tissue was considerable. Complete vascular shut-down was observed in the tumour 2 h after therapy and in the surrounding tissues at 24 h. Circulation damage was associated with vascular spasm and occlusion probably due to thrombi formation. Oedema was notable, especially following PDT with 600 J cm-2 at 24 h p.i. Images Figure 1

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Reoxygenation of tumours in “sandwich” chambers

Cited by 35 publications

References 20 publications

Tumor hypoxia: its impact on cancer therapy

Tumor hypoxia: its impact on cancer therapy

New Model for the Study of Angiogenesis and Antiangiogenesis in the Chick Embryo Chorioallantoic Membrane: The Gelatin Sponge/ Chorioallantoic Membrane Assay

Fluorescence and photodynamic effects of bacteriochlorin a observed in vivo in 'sandwich' observation chambers

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