Kirpatovskiĭ V I, Nadtochiĭ O N, Stepina N I, Kuznetsov V M, Obukhova T V
Urol Nefrol (Mosk). 1991 Nov-Dec(6):29-35.
Functional changes in the kidney exposed to 1-hour ischemia with surface cooling to +5+7 degrees C (series I) or +16+18 degrees C (series II) were studied in experiments on 50 rabbits and 20 non-inbred rats. In series II animals significant changes in renal function were not registered. In series I cooling there was a marked decrease of creatinine clearance, clearance of osmotic substances and Na-reabsorption during 1-3 days after ischemia. Dynamic scintigraphy with 131I-hyppuran revealed a decline in radionuclide secretion in series I that was more pronounced on day 14. In series II the time course of accumulation and excretion of 131I-hyppuran was almost normal. The worsening of renal function in series I experiments was accompanied with reduction of renal blood flow and activation of cell membrane lipid peroxidation. The investigation of the dependence of renal tissue impedance on the temperature that reflects thermotropic response of cell membrane structural organization showed phasic transitions of membrane lipids at the temperature below +13+14 degrees C. The findings indicate that for prolonged discontinuation of renal blood flow demanding deep kidney cooling, it is necessary to develop specific measures of protection against detrimental action of hypothermia.
在50只兔子和20只非近交系大鼠身上进行实验，研究肾脏在表面冷却至+5至+7摄氏度（系列I）或+16至+18摄氏度（系列II）的情况下暴露于1小时缺血时的功能变化。在系列II的动物中，未记录到肾功能的显著变化。在系列I的冷却过程中，缺血后1至3天肌酐清除率、渗透物质清除率和钠重吸收明显下降。用131I-马尿酸进行的动态闪烁扫描显示，系列I中放射性核素分泌下降，在第14天更为明显。在系列II中，131I-马尿酸的积累和排泄时间进程几乎正常。系列I实验中肾功能的恶化伴随着肾血流量的减少和细胞膜脂质过氧化的激活。对反映细胞膜结构组织热致反应的肾组织阻抗与温度的依赖性研究表明，在低于+13至+14摄氏度的温度下，膜脂会发生相变。研究结果表明，对于需要深度肾脏冷却的长时间肾血流中断，有必要制定针对低温有害作用的具体保护措施。
