论文部分内容阅读
经尾静脉给雄性昆明小鼠注入HpD(10mg/kg体重),48小时后阻断肾动脉,造成缺血、缺氧的肾脏模型。然后用250—300J/cm~2剂量的630nm波长激光照射小鼠肾脏。最早出现的形态学改变是间质水肿和毛细血管破坏。近端小管上皮细胞在光照后6小时出现形态学改变,其它结构均在光照后24小时发生坏死。超微结构主要是线粒体、内质网和细胞核的破坏。肾酶的损伤程度为Cytox>AKP>ACP>SDH。实验结果表明,断血肾脏对血卟啉光动力学作用敏感性降低,但血管损伤加重。因此,血管损伤不是造成实质细胞损伤的始动因素,氧在血卟啉光动力学作用中是必需的。
Male Kunming mice were injected with HpD (10 mg/kg body weight) via the tail vein and the renal artery was blocked 48 hours later, resulting in a model of ischemia and hypoxia. The mouse kidney was then irradiated with a 630 nm wavelength laser at a dose of 250-300 J/cm-2. The earliest morphological changes were interstitial edema and capillary destruction. Morphological changes occurred in the proximal tubule epithelial cells 6 hours after light exposure, and other structures were necrotic at 24 hours after light irradiation. The ultrastructure is mainly the destruction of mitochondria, endoplasmic reticulum and nuclei. The degree of renal enzyme damage was Cytox>AKP>ACP>SDH. The experimental results showed that the sensitivity of the blood-broken kidney to the photodynamic effects of hematoporphyrin was reduced, but the vascular injury was aggravated. Therefore, vascular injury is not the initiating factor that causes parenchymal cell injury. Oxygen is required in the photodynamic effect of hematoporphyrin.