Braunschweiger P G, Reynolds K, Nelson T R, Maring E
Department of Experimental Therapeutics, AMC Cancer Research Center, Denver, Colorado 80214.
Magn Reson Imaging. 1987;5(6):483-92. doi: 10.1016/0730-725x(87)90383-3.
The present experiments were conducted to determine the effects of dexamethasone mediated changes in tumor water distribution on proton relaxation times (T1, T2) in a murine pancreatic adenocarcinoma (Panc02). Spin lattice (T1) and spin-spin(T2) relaxation times were determined by ex vivo methods (10 MHz) and by in vivo imaging techniques (6.25 MHz) at various intervals after single or multiple dexamethasone treatments. In complementary studies, dexamethasone mediated changes in tumor capillary permeability, tumor water distribution, relative tumor blood flow and tumor cell proliferation were also determined. Proton spin lattice (T1) and spin-spin (T2 relaxation times for Panc02 tumors shortened within two hours of a single dexamethasone treatment. The time course and magnitude of this response was dexamethasone dose dependent. The time dependent changes in T1 and T2 after dexamethasone were similar at 10 MHz (ex vivo) and 6.25 MHz (in vivo imaging). Although dexamethasone produced little or no change in total tumor water content and tumor cell proliferation, transient changes in the physiologic distribution of tumor water were clearly demonstrated. The data supports the idea that dexamethasone induced changes in the distribution of tumor water were mediated by changes in capillary permeability and tumor blood flow. These physiologic responses produced serial changes in tumor extracellular extravascular water content that were consistent with the observed changes in tumor T1 and T2. The results from these experiments might imply that therapy associated changes in tumor proton relaxation times may not only reflect changes in tissue water content, but may also reflect physiologic responses which alter the distribution of tissue water and solute.
进行本实验以确定地塞米松介导的肿瘤水分分布变化对小鼠胰腺腺癌（Panc02）质子弛豫时间（T1、T2）的影响。在单次或多次地塞米松治疗后的不同时间间隔，通过离体方法（10 MHz）和体内成像技术（6.25 MHz）测定自旋晶格（T1）和自旋 - 自旋（T2）弛豫时间。在补充研究中，还测定了地塞米松介导的肿瘤毛细血管通透性、肿瘤水分分布、相对肿瘤血流和肿瘤细胞增殖的变化。单次地塞米松治疗后两小时内，Panc02肿瘤的质子自旋晶格（T1）和自旋 - 自旋（T2）弛豫时间缩短。这种反应的时间进程和幅度呈地塞米松剂量依赖性。地塞米松处理后T1和T2的时间依赖性变化在10 MHz（离体）和6.25 MHz（体内成像）时相似。尽管地塞米松对肿瘤总含水量和肿瘤细胞增殖几乎没有影响或没有影响，但肿瘤水分的生理分布发生了明显的瞬时变化。数据支持这样的观点，即地塞米松诱导的肿瘤水分分布变化是由毛细血管通透性和肿瘤血流的变化介导的。这些生理反应导致肿瘤细胞外血管外含水量发生一系列变化，这与观察到的肿瘤T1和T2变化一致。这些实验结果可能意味着与治疗相关的肿瘤质子弛豫时间变化不仅可能反映组织含水量的变化，还可能反映改变组织水分和溶质分布的生理反应。
