Johnson G, Bond R F, Stack L B, Class C A, Hardebeck J R
Circ Shock. 1987;21(3):233-45.
The compensatory cardiovascular response to hemorrhage includes a baroreceptor-induced activation of the sympathetic nervous system resulting in an attempt to reestablish MAP through peripheral vasoconstriction. If the hypotension is not reversed this compensatory vasoconstriction will progress to a loss of vascular tone known as vascular decompensation. The primary purpose of the present study was to compare the effectiveness of military antishock trousers (MAST) applied during the compensatory and decompensatory stages of hemorrhagic hypotension. MAST pressures of 30, 50, 70, and 90 mm Hg were applied during control, compensation, and decompensation. The results showed that MAST pressures up to 90 mm Hg were ineffective at raising mean arterial blood pressure (MAP) when applied to normotensive dogs; MAP increased 62% when MAST were applied during compensation as the result of a significant augmentation of cardiac output (stroke volume and heart rate) with no change in TPR; and a modest increase in MAP from 40 to 55 mm Hg occurred when MAST pressure was increased to 70 mm Hg during decompensation, which was accounted for entirely on the basis of an increased total peripheral resistance with no significant change in CO.
对出血的代偿性心血管反应包括压力感受器诱导的交感神经系统激活，试图通过外周血管收缩来重建平均动脉压（MAP）。如果低血压得不到纠正，这种代偿性血管收缩将发展为血管张力丧失，即所谓的血管失代偿。本研究的主要目的是比较在出血性低血压的代偿期和失代偿期应用军事抗休克裤（MAST）的效果。在对照、代偿和失代偿期间分别施加30、50、70和90 mmHg的MAST压力。结果表明，对正常血压的犬施加高达90 mmHg的MAST压力对提高平均动脉血压（MAP）无效；在代偿期应用MAST时，MAP增加62%，这是由于心输出量（每搏量和心率）显著增加而总外周阻力（TPR）无变化所致；在失代偿期将MAST压力增加到70 mmHg时，MAP从40 mmHg适度增加到55 mmHg，这完全是由于总外周阻力增加而心输出量（CO）无显著变化所致。
