Mathis Keisa W, Zambell Kirsten, Olubadewo Joseph O, Molina Patricia E
Department of Physiology, LSU Health Sciences Center, New Orleans, LA 70112, USA.
Shock. 2006 Jul;26(1):55-61. doi: 10.1097/01.shk.0000215320.06866.30.
The incidence of traumatic injury, frequently associated with hemorrhagic shock, is higher in the alcohol-intoxicated individual. The outcome, as it pertains to both morbidity and mortality of this population, is partly dependent on duration of alcohol exposure and levels of blood alcohol at time of injury. In previous studies, we demonstrated that prolonged alcohol intoxication (15-h duration) produces marked hemodynamic instability and exacerbated early lung proinflammatory cytokine expression after hemorrhagic shock. The present study examines whether a shorter and more modest period of alcohol intoxication is sufficient to alter hemodynamic and proinflammatory responses to hemorrhagic shock. Chronically instrumented, conscious male Sprague-Dawley rats (250-300 g) received a single intragastric bolus of alcohol (1.75 g/kg) 30 min before the administration of fixed-volume (50%) hemorrhagic shock, followed by fluid resuscitation with Ringer lactate. Time-matched controls were administered on isocaloric dextrose bolus (3 g/kg). Alcohol (blood alcohol concentration, 152 +/- 10 mg/dL) produced a 14% decrease in basal mean arterial blood pressure and a more profound hypotensive response to equal blood loss. The 2-fold rise in circulating norepinephrine levels was similar in alcohol- and dextrose-treated hemorrhaged animals despite greater hypotension in alcohol-treated animals. Significant upregulation in lung and spleen interleukin (IL) 1, IL-6, IL-10, and tumor necrosis factor alpha expression was observed immediately after hemorrhage and fluid resuscitation, as previously reported. Only the hemorrhage-induced rise in lung IL-6 and tumor necrosis factor alpha was prevented by alcohol administration. In contrast, spleen cytokine responses to hemorrhage were not altered by alcohol administration. These results indicate that moderate acute alcohol intoxication results in significant modulation of hemodynamic and neuroendocrine responses to hemorrhagic shock.
创伤性损伤的发生率在酒精中毒个体中较高，且常伴有失血性休克。就该人群的发病率和死亡率而言，其结果部分取决于酒精暴露的持续时间和受伤时的血液酒精水平。在先前的研究中，我们证明长时间酒精中毒（持续15小时）会导致明显的血流动力学不稳定，并在失血性休克后加剧早期肺部促炎细胞因子的表达。本研究旨在探讨较短且适度的酒精中毒时间是否足以改变对失血性休克的血流动力学和促炎反应。对长期植入仪器的清醒雄性Sprague-Dawley大鼠（250-300克）在给予固定体积（50%）失血性休克前30分钟给予单次胃内酒精推注（1.75克/千克），随后用乳酸林格液进行液体复苏。时间匹配的对照组给予等热量的葡萄糖推注（3克/千克）。酒精（血液酒精浓度，152±10毫克/分升）使基础平均动脉血压降低14%，对等量失血产生更显著的低血压反应。尽管酒精处理的动物低血压更严重，但酒精和葡萄糖处理的出血动物循环去甲肾上腺素水平的两倍升高相似。如先前报道，在出血和液体复苏后立即观察到肺和脾白细胞介素（IL）1、IL-6、IL-10和肿瘤坏死因子α表达显著上调。只有酒精给药可预防出血诱导的肺IL-6和肿瘤坏死因子α升高。相比之下，酒精给药未改变脾对出血的细胞因子反应。这些结果表明，中度急性酒精中毒会显著调节对失血性休克的血流动力学和神经内分泌反应。
