Murakawa K, Izumi R, Kobayashi A
Department of Anesthesiology, Hyogo College of Medicine, Hyogo, Japan.
J Anesth. 1989 Mar 1;3(1):10-5. doi: 10.1007/s0054090030010.
To evaluate the development of renal hypoxia during hemorrhagic shock, fourteen dogs were induced in this study. The animals were divided equally into a group in which mean arterial pressure (MAP) was kept at 50 mmHg (group 1), and into another where MAP was kept at 40 mmHg for 180 min (group 2). Renal tissue gas tensions were determined by a mass spectrometer. In the 50-mmHg group, renal tissue oxygen tension (PrO2) dropped for 15 min following hemorrhage, remained constant for 90 min, then fell further for 150 min before a plateau was established. In the 40-mmHg group, the PrO2 dropped for 90 min before reaching a plateau. The second PrO2 decline occurred at the same level in both the 50-mmHg group and the 40-mmHg group. The point at which the same PrO2 level occurred for each group suggests the cessation of oxygen consumption and the conditions of renal hypoxia. It is assumed that renal hypoxia occurs in 120 min at a MAP of 50-mmHg and in 60 min at a MAP of 40 mmHg.
为评估失血性休克期间肾缺氧的发展情况,本研究诱导了14只犬。动物被平均分为两组,一组平均动脉压(MAP)维持在50 mmHg(第1组),另一组MAP维持在40 mmHg并持续180分钟(第2组)。通过质谱仪测定肾组织气体张力。在50 mmHg组,出血后肾组织氧张力(PrO2)下降15分钟,保持恒定90分钟,然后在达到平台期前进一步下降150分钟。在40 mmHg组,PrO2在达到平台期前下降90分钟。50 mmHg组和40 mmHg组的第二次PrO2下降发生在相同水平。每组出现相同PrO2水平的时间点提示氧消耗停止及肾缺氧情况。假定在MAP为50 mmHg时肾缺氧在120分钟时发生,在MAP为40 mmHg时肾缺氧在60分钟时发生。