Lund N, de Asla R J, Cladis F, Papadakos P J, Thorborg P A
Department of Anesthesiology, University of Rochester Medical Center, NY 14642, USA.
J Trauma. 1995 May;38(5):767-75. doi: 10.1097/00005373-199505000-00016.
It has been suggested that septic shock is a disorder of microvascular autoregulation. Tissue blood flow is modulated by the state of activation of upstream endothelial receptors controlling the vascular smooth muscle tone. Because vascular receptor populations vary between organs, it should be expected that vasoactive drugs affect tissue oxygenation differently in different organs. We studied the effects of dopexamine HCl (a novel inotrope) and septic shock on oxygen delivery as well as tissue Po2 in gut, liver, and skeletal muscle in anesthetized rabbits. Employing the thermodilution technique, cardiac output was measured across the pulmonary bed and used to calculate oxygen delivery. Three eight-channel Mehrdraht Dortmund Oberfläche oxygen electrodes were placed on gut serosa, liver, and skeletal muscle surfaces, respectively, and sufficient readings were obtained to calculate tissue Po2 distributions. During septic shock mean arterial pressure, cardiac output, oxygen delivery, and mean tissue Po2 decreased in all organs. Our results suggest that the observed changes in tissue oxygenation during septic shock were caused by defective regulation of microvascular blood flow. In conclusion, during baseline conditions dopexamine HCl caused no statistically significant changes in tissue oxygenation in any organ, except in skeletal muscle at 10 micrograms/kg/min when tissue Po2 increased. During septic shock, however, dopexamine HCl improved oxygenation in all three organs in a dose-dependent manner.
有人提出，感染性休克是一种微血管自动调节紊乱。组织血流受控制血管平滑肌张力的上游内皮受体激活状态的调节。由于不同器官的血管受体群体不同，因此可以预期血管活性药物对不同器官的组织氧合作用会有所不同。我们研究了盐酸多培沙明（一种新型的正性肌力药物）和感染性休克对麻醉兔肠道、肝脏和骨骼肌的氧输送以及组织氧分压的影响。采用热稀释技术，测量通过肺床的心输出量，并用于计算氧输送。分别在肠道浆膜、肝脏和骨骼肌表面放置三个八通道Mehrdraht Dortmund Oberfläche氧电极，并获得足够的读数以计算组织氧分压分布。在感染性休克期间，所有器官的平均动脉压、心输出量、氧输送和平均组织氧分压均下降。我们的结果表明，感染性休克期间观察到的组织氧合变化是由微血管血流调节缺陷引起的。总之，在基线条件下，盐酸多培沙明除了在10微克/千克/分钟时骨骼肌组织氧分压升高外，在任何器官中均未引起组织氧合的统计学显著变化。然而，在感染性休克期间，盐酸多培沙明以剂量依赖的方式改善了所有三个器官的氧合。
