Photodynamic effect of haematoporphyrin on blood microcirculation

Castelani, A.; Pace, G.; Concioli, M.

doi:10.1002/path.1700860111

Cited by 60 publications

(23 citation statements)

References 2 publications

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“…mitochondria (Grossweiner, 1984), and by damage to the tumour vasculature leading to secondary tumour cell death (Castellani et al, 1963;Bugelski et al, 1981;Star et al, 1986 (Baas et al, 1994), where the maximum benefit from the combination MMC + PDT is obtained when the drug is given before illumination. This difference may be due to the higher light dose (400 J cm-') required for effective tumour treatment with Photofrin-mediated PDT.…”

Section: Resultsmentioning

confidence: 99%

Mechanisms for optimising photodynamic therapy: second-generation photosensitisers in combination with mitomycin C

Geel

Oppelaar²,

Oussoren³

et al. 1995

Br J Cancer

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Section: Resultsmentioning

confidence: 99%

Mechanisms for optimising photodynamic therapy: second-generation photosensitisers in combination with mitomycin C

Geel

Oppelaar²,

Oussoren³

et al. 1995

Br J Cancer

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“…McIlroy et al (1998) described a 10-fold decrease of the oxygen level in normal rat liver following PDT with ALA (100 mW, 60 J) (McIlroy et al, 1998). The decline of pO 2 following PDT could be caused by photochemical consumption of molecular oxygen (Busch et al, 2000) or by the lack of oxygen supply caused by massive microvascular damage following high-dose PDT (Castellani et al, 1963;Vaupel et al, 1977Vaupel et al, , 1981Vaupel et al, , 1989. The fragile microvasculature of experimental and human solid tumours is characterised already in very early growth stages by structural and functional abnormalities (Vaupel et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Effects of light fractionation and different fluence rates on photodynamic therapy with 5-aminolaevulinic acid in vivo

et al. 2003

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To improve efficacy of photodynamic therapy (PDT) with intravenously administered 5-aminolaevulinic acid (ALA) fractionating the light dose or reducing the light intensity may be a possibility. Therefore, Syrian Golden hamsters were fitted with dorsal skinfold chambers containing an amelanotic melanoma (n ¼ 26). PDT was performed (100 mW cm À2 , 100 J cm À2 , continuously or fractionated, and 25 mW cm À2 , 100 J cm À2 ; continuously or fractionated) using an incoherent light source following i.v. application of ALA. Following fractionated irradiation, the light was paused after 20 J cm À2 for 15 min. Prior to and up to 24 h after PDT tissue, pO 2 was measured using luminescence lifetime imaging. The efficacy was evaluated by measuring the tumour volume of amelanotic melanoma cells grown subcutaneously in the back of Syrian Golden hamsters (n ¼ 36). Only high-dose PDT resulted in a significant decrease of pO 2 . Irrespective of the mode of irradiation only high-dose PDT induced complete remission of all tumours (13 out of 13). It could be shown that low-dose PDT failed to induce a significant decrease of pO 2 . No significant effect of fractionated irradiation was shown regarding the therapeutic efficacy 28 days after PDT. Thus performing a fractionated PDT with ALA or reducing the light intensity seems not to be successful in clinical PDT according to the present data.

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“…It is concluded that angiogenesis-plays an important role in vascular recovery following PDT. There is increasing evidence that, in vivo, the vasculature both of tumours and normal tissues is promptly damaged by PDT. Castellani et al (1963) observed microagglutination of the red blood cells in the tongues of live frogs 5 min after exposure to light, following injection of haematoporphyrin hydrochloride. Similarly Star et al (1986), using HPD, observed early damage to blood vessels in rat mammary tumours grown in sandwich observation chambers.…”

mentioning

confidence: 99%

“…There is increasing evidence that, in vivo, the vasculature both of tumours and normal tissues is promptly damaged by PDT. Castellani et al (1963) (Bugelski et al, 1981). This has also been found to occur in normal tissue following PDT, by Zhou et al (1985) in mouse skin, and by Berenbaum et al (1986) in the brains of mice.…”

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confidence: 99%

Quantitative histological changes in murine tail skin following photodynamic therapy

Benstead

Moore²

1989

Br J Cancer

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Summary Mice were treated by an intravenous injection of 2 mg of the photosensitising drug meso-tetra (sulphonatophenyl) porphine (TPPS) and 24 h later a 2.5cm length of their tails was exposed to visible light (photodynamic therapy, PDT). Using cross-sections from the centre of the treatment field, the absolute areas occupied by epidermis, dermis, hypodermis, tendon and bone, and also the total number and area of the blood vessels in the dermis and hypodermis, were compared between control and PDT-treated animals. There was a significant increase in the mean cross-sectional area of the epidermis, dermis and hypodermis following both 90Jcm-2 (a dose expected to produce a low incidence of tail necrosis) and 180Jcm-2 (expected to produce a 100% tail necrosis rate), on day 1 and day 5 following light exposure. The cross-sectional area of the vascular compartment was also significantly increased by day 5 at both dose levels. Differences were observed between the two doses when the total number of blood vessels were compared. There was a significant increase in the number of blood vessels by day 5 following 90Jcm-2 in both the dermis and hypodermis, but not following 180JCcm-2. This appeared to be due to a significant increase in blood vessels with a cross-sectional area of <100 jIm2 by day 5 at the lower dose. It is concluded that angiogenesis-plays an important role in vascular recovery following PDT. There is increasing evidence that, in vivo, the vasculature both of tumours and normal tissues is promptly damaged by PDT. Castellani et al. (1963) (Bugelski et al., 1981). This has also been found to occur in normal tissue following PDT, by Zhou et al. (1985) in mouse skin, and by Berenbaum et al. (1986) in the brains of mice.Functional studies following PDT support these histological findings. Oxygen microelectrode measurements performed by Bicher et al. (1981) found a profound reduction in oxygen tension in a mouse mammary carcinoma within one hour of light exposure. Selman et al. (1985) demonstrated a significant decrease in blood flow to rat jejunum 10 min after PDT using a radioactive microscope technique. All these studies used HPD as the photosensitiser.Determination of blood flow in murine tail skin using the xenon clearance method, in animals treated with light 24h after exposure to the hydrophilic sensitiser TPPS, also revealed a significant decrease within 10min (Benstead & Moore, 1988a). We also observed recovery of blood flow between the first and fifth days after treatment with light doses below those that produced necrosis of the tail.Whether necrosis (defined here as complete loss of the tail distal to the proximal edge of the light beam) occurred in individual animals, following administration of a dose of PDT which produced a 50% incidence of necrosis, appeared to depend on the timing and degree of this recovery rather than the extent of the initial impairment of blood flow. The time course of this recovery also appeared to be important in determining the response of murine tail skin to a fract...

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Photodynamic effect of haematoporphyrin on blood microcirculation

Cited by 60 publications

References 2 publications

Mechanisms for optimising photodynamic therapy: second-generation photosensitisers in combination with mitomycin C

Mechanisms for optimising photodynamic therapy: second-generation photosensitisers in combination with mitomycin C

Effects of light fractionation and different fluence rates on photodynamic therapy with 5-aminolaevulinic acid in vivo

Quantitative histological changes in murine tail skin following photodynamic therapy

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