Schloerb P R, Sieracki L, Botwin A J, Winblad J M, Maguire M H
Am J Physiol. 1981 Jan;240(1):R52-60. doi: 10.1152/ajpregu.1981.240.1.R52.
The effect of intravenous (iv) infusion of 6.25 mumol of ATP-MgCl2 on survival and tissue ATP levels in hemorrhagic shock was investigated using a rat model. Mortality in ATP-MgCl2-treated shocked rats was 50% compared with 53% in saline-treated controls. Tissue ATP levels in ATP-MgCl2-treated shocked rats did not differ from those in saline-treated shocked rats nor from those in sham-operated controls. After iv infusion of 6.25 mumol of [8-14C]ATP-MgCl2, shocked, sham-operated, and nephrectomized rats had similar tissue distributions of 14C. The 14C in heart, lung, kidney, and liver of shocked and sham-operated rats was present almost entirely as nonphosphorylated [8-14C]ATP catabolites. It is concluded that ATP-MgCl2 iv did not benefit survival or enhance tissue ATP levels in shocked animals and that the administered ATP was rapidly and extensively degraded.
使用大鼠模型研究了静脉输注6.25 μmol ATP - MgCl₂对失血性休克大鼠存活率和组织ATP水平的影响。经ATP - MgCl₂治疗的休克大鼠死亡率为50%，而生理盐水治疗的对照组为53%。经ATP - MgCl₂治疗的休克大鼠的组织ATP水平与生理盐水治疗的休克大鼠以及假手术对照组的水平无差异。静脉输注6.25 μmol [8 - ¹⁴C]ATP - MgCl₂后，休克、假手术和肾切除大鼠的¹⁴C组织分布相似。休克和假手术大鼠心脏、肺、肾和肝脏中的¹⁴C几乎完全以非磷酸化的[8 - ¹⁴C]ATP分解代谢产物形式存在。得出的结论是，静脉注射ATP - MgCl₂对休克动物的存活率没有益处，也不会提高组织ATP水平，并且所给予的ATP会迅速且广泛地降解。
