Wood C D, Bentz Y, Mullaney C, Daniel A M
J Surg Res. 1985 Jan;38(1):1-6. doi: 10.1016/0022-4804(85)90002-2.
To investigate the temporal relationship of changes in carbohydrate metabolism to changes in the hemodynamic stability of the dog in protracted hemorrhagic shock, 30 animals were studied. Blood pressure was maintained at 60 mm Hg for 12 hr during which hemodynamic and metabolic parameters were studied. In early shock cardiac output was decreased and peripheral resistance increased. After 2 hr cardiac output began to increase and peripheral resistance began a progressive decline despite the continuing hypotensive state. Hemodynamic decompensation was essentially complete at 5 hr. There was early and marked mobilization of carbohydrate stores. Muscle glycogen was rapidly mobilized over a 5-hr period. Serum glucose and blood lactate levels rose and remained elevated for 8 hr. Amino acid degradation remained at high levels throughout the experimental period. Hemodynamic decompensation began well before significant depletion of carbohydrate stores and was complete well before the relative exhaustion of the available reserves.
为了研究长期失血性休克时犬碳水化合物代谢变化与血流动力学稳定性变化之间的时间关系,对30只动物进行了研究。将血压维持在60毫米汞柱12小时,在此期间研究血流动力学和代谢参数。休克早期心输出量降低,外周阻力增加。2小时后,尽管持续处于低血压状态,但心输出量开始增加,外周阻力开始逐渐下降。5小时时血流动力学失代偿基本完成。碳水化合物储备早期即有明显动员。肌肉糖原在5小时内迅速动员。血清葡萄糖和血乳酸水平升高并持续8小时。整个实验期间氨基酸降解一直处于高水平。血流动力学失代偿在碳水化合物储备显著耗竭之前就已开始,并且在可用储备相对耗尽之前就已完成。