论文部分内容阅读
一、升压化疗的机制 肿瘤化疗的效果取决于抗肿瘤药物到达瘤组织的浓度(C)和作用时间(T)的乘积值,即C×T值。多数抗肿瘤药物的作用缺乏选择性,在杀灭癌细胞的的同时对机体的正常组织如骨髓,胃肠道等也具有不同程度的损害作用。因此,提高肿瘤化疗疗效的关键在于增加药物到达癌组织的选择性,从而最大限度的杀伤癌细胞,最大限度地保护正常组织。1976年,佐藤,铃木等通过动物实验发现,肿瘤血管的机能与正常组织血管明显不同。当给健康大白鼠静脉内持续投予血管收缩剂血管紧张素Ⅱ(AT—Ⅱ),使血压上升至一定范围(平均动脉压在150mmHg左右)时,鼠的肝,脑,骨髓的血流量基本上保持恒定,皮肤及肾脏的血流量减少。而荷瘤鼠(吉田腹水肝癌)静脉内持续给予AT—Ⅱ收缩血管产生高血压状态时,肝及骨髓血流量无变化,
First, the mechanism of booster chemotherapy The effect of tumor chemotherapy depends on the concentration (C) of the antitumor drug reaching the tumor tissue (C) and the action time (T), that is, the C×T value. The role of most anti-cancer drugs is lack of selectivity, and they also have different degrees of damage to the normal tissues of the body such as bone marrow and gastrointestinal tract while killing cancer cells. Therefore, the key to improving the efficacy of cancer chemotherapy is to increase the selectivity of the drug to reach the cancer tissue, so as to maximize the killing of cancer cells and maximize the protection of normal tissues. In 1976, Sato, Suzuki and other animal experiments found that the function of tumor blood vessels and normal tissue blood vessels are significantly different. When healthy rats continue to be administered intravenously with the vasoconstrictor angiotensin II (AT-II) to increase the blood pressure to a certain range (average arterial pressure is around 150 mmHg), the blood flow of the liver, brain, and bone marrow of rats is basically the same. Keeping it constant, blood flow to the skin and kidneys decreases. However, when the tumor-bearing mice (Yoshita ascites liver cancer) continued to give AT-II contraction of blood vessels to produce hypertension, there was no change in the blood flow of the liver and bone marrow.