Jellinek M, Chandel B, Abdulla R, Shapiro M J, Baue A E
Department of Surgery, St. Louis University School of Medicine, Missouri 63104.
Experientia. 1992 Oct 15;48(10):980-5. doi: 10.1007/BF01919146.
Oxidation-reduction (redox) potential measurements were made in the blood of rabbits subjected to hemorrhagic shock followed by treatment with a mild oxidizing agent (albumin). Control redox potential reading corrected for pH was -8.8 +/- 1.3 millivolts (mV) in arterial blood (A) and -18.0 +/- 2.0 mV in venous blood (V). This A-V difference indicated that hydrogen equivalents coming from muscle and other tissues were partially consumed in the lungs. A 20-mV drop on the V and a 13 mV on the A side was seen after shock. This did not fully return to control 2 h after return of the shed blood. Infusion of 2 g of albumin/kg/h raised the V redox potential to control, but it returned to untreated levels when the albumin was discontinued. The reductive load imposed on the animal by shock appeared to be large and not readily reversed by reperfusion or by the quantity of albumin given. Thus, it may be concluded that cellular respiration had not been adequately restored. This reductive load may impede recovery by suppression of cellular respiration and other cell and organ functions.
对经历失血性休克后用轻度氧化剂（白蛋白）治疗的家兔血液进行了氧化还原电位测量。经pH校正的对照氧化还原电位读数在动脉血（A）中为-8.8±1.3毫伏（mV），在静脉血（V）中为-18.0±2.0 mV。这种动静脉差异表明来自肌肉和其他组织的氢当量在肺部被部分消耗。休克后，静脉侧下降20 mV，动脉侧下降13 mV。在回输 shed blood 2小时后，这并未完全恢复到对照水平。以2 g白蛋白/千克/小时的速度输注可使静脉氧化还原电位恢复到对照水平，但停止输注白蛋白后又回到未治疗水平。休克给动物带来的还原负荷似乎很大，再灌注或给予的白蛋白量都不易将其逆转。因此，可以得出结论，细胞呼吸尚未得到充分恢复。这种还原负荷可能通过抑制细胞呼吸以及其他细胞和器官功能来阻碍恢复。
