Geraci J P, Jackson K L, Mariano M S
Department of Environmental Health, School of Public Health and Community Medicine, University of Washington, Seattle 98195.
Radiat Res. 1987 Sep;111(3):518-32.
Whole-body and organ fluid compartment sizes and plasma sodium concentrations were measured in conventional, GI decontaminated, bile duct ligated, and choledochostomized rats at different times after various doses of gamma radiation. In addition, sodium excretion was measured in rats receiving lethal intestinal radiation injury. After doses which were sublethal for 3-5 day intestinal death, transient decreases occurred in all the fluid compartments measured (i.e., total body water, extracellular fluid space, plasma volume). No recovery of these fluid compartments was observed in rats destined to die from intestinal radiation injury. The magnitude of the decreases in fluid compartment sizes was dose dependent and correlated temporally with the breakdown and recovery of the intestinal mucosa but was independent of the presence or absence of enteric bacteria or bile acids. Associated with the loss of fluid was an excess excretion of 0.83 meq of sodium between 48 and 84 h postirradiation. This represents approximately 60% of the sodium lost from the extracellular fluid space in these animals during this time. The remaining extracellular sodium loss was due to redistribution of sodium to other spaces. It is concluded that radiation-induced breakdown of the intestinal mucosa results in lethal losses of fluid and sodium as evidenced by significant decreases in total body water, extracellular fluid space, plasma volume, and plasma sodium concentration, with hemoconcentration. These changes are sufficient to reduce tissue perfusion leading to irreversible hypovolemic shock and death.
在给予不同剂量γ射线照射后的不同时间,对常规、胃肠道去污、胆管结扎和胆总管造口的大鼠测量了全身和器官体液腔室大小以及血浆钠浓度。此外,还对接受致死性肠道辐射损伤的大鼠测量了钠排泄。在对3 - 5天肠道死亡为亚致死剂量后,所测量的所有体液腔室(即总体液、细胞外液间隙、血浆容量)均出现短暂下降。在注定死于肠道辐射损伤的大鼠中,未观察到这些体液腔室的恢复。体液腔室大小下降的幅度与剂量相关,并在时间上与肠黏膜的破坏和恢复相关,但与肠道细菌或胆汁酸的存在与否无关。与液体丢失相关的是,照射后48至84小时内钠过量排泄0.83毫当量。这约占这段时间内这些动物细胞外液间隙钠丢失量的60%。其余的细胞外钠丢失是由于钠重新分布到其他空间。结论是,辐射诱导的肠黏膜破坏导致液体和钠的致死性丢失,表现为总体液、细胞外液间隙、血浆容量和血浆钠浓度显著下降,并伴有血液浓缩。这些变化足以减少组织灌注,导致不可逆的低血容量性休克和死亡。