Noshima S, Noda H, Herndon D N, Traber L D, Traber D L
Department of Anesthesiology, University of Texas Medical Branch, Galveston.
J Appl Physiol (1985). 1993 Apr;74(4):1528-33. doi: 10.1152/jappl.1993.74.4.1528.
Cardiac function was studied in an unanesthetized ovine model of hyperdynamic endotoxemia. Sixteen sheep were instrumented with ultrasonic crystals on the left ventricle to measure changes in its external diameter, a pressure transducer in the left ventricle, and aortic and Swan-Ganz catheters. The animals received either Escherichia coli endotoxin [lipopolysaccharide (LPS), 10 ng.kg-1.min-1; LPS group, n = 10] or an equivalent amount of 0.9% NaCl (sham group, n = 6). Between 1 and 8 h after LPS, a hypodynamic state with low cardiac output ensued (LPS 5.0 +/- 0.2 vs. sham 6.3 +/- 0.4 l.min-1.m-2). During this period, the end-systolic pressure-diameter relationship, a sensitive index of myocardial contractility, was reduced (LPS 10.4 +/- 1.2 vs. sham 17.2 +/- 0.8 mmHg/mm). After this first phase, the sheep developed a persistent hyperdynamic state characterized by a significant increase in cardiac output. By 24 h after LPS administration, the cardiac output was 10.1 +/- 0.5 l.min-1.m-2 (sham 6.3 +/- 0.3). Despite the marked elevation of cardiac output, the end-systolic pressure-diameter relationship had fallen to 8.5 +/- 0.9 mmHg/mm (sham 16.0 +/- 1.2). In a model of hyperdynamic state, an increased cardiac output occurs despite a significant depression in myocardial contractility.
在未麻醉的高动力性内毒素血症绵羊模型中研究心脏功能。16只绵羊在左心室安装超声晶体以测量其外径变化，在左心室安装压力传感器，并插入主动脉和 Swan-Ganz 导管。动物们分别接受大肠杆菌内毒素[脂多糖（LPS），10 ng·kg-1·min-1；LPS组，n = 10]或等量的0.9%氯化钠（假手术组，n = 6）。在给予LPS后1至8小时内，出现心输出量低的低动力状态（LPS为5.0±0.2 vs.假手术组为6.3±0.4 l·min-1·m-2）。在此期间，反映心肌收缩力的敏感指标——收缩末期压力-直径关系降低（LPS为10.4±1.2 vs.假手术组为17.2±0.8 mmHg/mm）。在第一阶段之后，绵羊出现持续的高动力状态，其特征是心输出量显著增加。到给予LPS后24小时，心输出量为10.1±0.5 l·min-1·m-2（假手术组为6.3±0.3）。尽管心输出量显著升高，但收缩末期压力-直径关系已降至8.5±0.9 mmHg/mm（假手术组为16.0±1.2）。在高动力状态模型中，尽管心肌收缩力明显降低，但心输出量仍增加。
