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Mechanisms of tumor necrosis in photodynamic therapy with a chlorine photosensitizer: experimental studies

机译:氯光敏剂光动力疗法中肿瘤坏死的机制:实验研究

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A photodynamic therapy experiment on 118 inbred white mice with transplanted Ehrlich's tumor (mouse mammary gland adenocarcinoma) is performed to reveal mechanisms of necrosis formation. In 7-10 days the tumor of 1-1.5 cm diameter is formed under skin at the injection point, and PDT procedure is applied. There were used a chlorine type photosensitizer Radachlorine? and 662 nm wavelength diode laser. The drug is injected by intravenously at the dose of 40 mg/kg; the irradiation is executed in 2-2.5 hours at the surface dose of about 200 J/cm2. Each of the mice had a photochemical reaction in form of destructive changes at the irradiation region with subsequent development of dry coagulation necrosis. After rejection of the necrosis there occurred epithelization of defect tissues in a tumor place. Histological investigations were conducted in different follow-up periods, in 5 and 30 min, 1, 3, 6, and 12 hours, 1, 3, 7 and 28 days after irradiation. They included optical microscopy, immune marker analysis, morphometry with measurements of volume density of epithelium, tumor stroma and necroses, vascular bed. The investigations showed that an important role in damaging mechanisms of photodynamic action belongs to hypoxic injuries of tumor mediated by micro vascular disorders and blood circulatory disturbances. The injuries are formed in a few stages: microcirculation angiospasm causing vessel paresis, irreversible stases in capillaries, diapedetic hemorrhages, thromboses, and thrombovasculitis. It is marked mucoid swelling and fibrinoid necrosis of vascular tissue. Progressive vasculitises result in total vessel obliteration and tumor necrosis.
机译:进行了118只近亲白小鼠移植的埃里希氏肿瘤(小鼠乳腺腺癌)的光动力疗法实验,以揭示坏死形成的机制。在7-10天之内,在注射点皮肤下会形成直径1-1.5 cm的肿瘤,并应用PDT程序。有没有使用过氯型光敏剂Radachlorine?和662 nm波长的二极管激光器。该药物以40 mg / kg的剂量静脉内注射;照射在2-2.5小时内以约200J / cm 2的表面剂量进行。每只小鼠在照射区域发生破坏性变化形式的光化学反应,随后发生干凝结坏死。坏死排除后,在肿瘤部位上皮出现了缺陷组织的上皮化。在照射后的1、5、30分钟,1、3、6和12小时,1、3、7和28天内,在不同的随访期间进行了组织学研究。他们包括光学显微镜,免疫标记物分析,形态学测量,测量上皮,肿瘤基质和坏死的体积密度,血管床。研究表明,在破坏光动力作用机制中的重要作用是由微血管疾病和血液循环障碍介导的肿瘤低氧损伤。损伤的形成分为几个阶段:微循环血管痉挛引起血管轻瘫,毛细血管不可逆转,尿道出血,血栓形成和血栓血管炎。它被标记为粘液样肿胀和血管组织纤维蛋白样坏死。进行性血管炎导致总血管闭塞和肿瘤坏死。

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