NONINVASIVE ASSESSMENT OF END-SYSTOLIC PRESSURE LENGTH AND STRESS SHORTENING RELATIONSHIPS IN NORMAL INDIVIDUALS - SIGNIFICANCE OF DIFFERENT LOADING CONDITIONS INDUCED BY METHOXAMINE AND ANGIOTENSIN-II
NONINVASIVE ASSESSMENT OF END-SYSTOLIC PRESSURE LENGTH AND STRESS SHORTENING RELATIONSHIPS IN NORMAL INDIVIDUALS - SIGNIFICANCE OF DIFFERENT LOADING CONDITIONS INDUCED BY METHOXAMINE AND ANGIOTENSIN-II
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DOI：
10.1093/oxfordjournals.eurheartj.a062175
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发表时间：
1987-10-01
影响因子：
39.3
通讯作者：
NIENABER, CA
中科院分区：
文献类型：
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作者：
HAUSDORF, G;GLUTH, J;NIENABER, CA
为了评估收缩末期压力-尺寸和应力-缩短关系是否受到用于其评估的药物的影响，我们分析了血管紧张素II（N=30）和甲氧胺（N=10）在正常个体中的作用。通过M型超声心动图进行左心室尺寸和壁厚度的系列测量;通过间接校准的颈动脉脉搏描记法评估收缩末期压。反映前负荷的舒张末期内径在使用血管紧张素II的后负荷激发期间保持不变，但使用甲氧胺时显著增加（P < 0.001）。收缩末期压力-尺寸关系（P < 0.0002）、收缩末期室壁应力与短轴缩短率关系（P <0.002）、收缩末期室壁应力与平均纤维短轴缩短速度关系（P <0.02）因所用造影剂而有显著差异。当使用血管紧张素II时，收缩末期压力为零时的外推收缩末期尺寸Do显著向左偏移（P < 0.02）;这被认为是由于其对前负荷的影响可忽略不计。我们的数据表明，收缩末期压力尺寸和应力缩短关系的评估显着依赖于药物的具体效果和变化的前负荷在后负荷的挑战。基于这些结果，强调使用血管紧张素II的收缩末期压力尺寸和应力缩短关系的评估。
To evaluate whether the end-systolic pressure-dimension and stress-shortening relations are influenced by the drugs used for their assessment, we analysed the effects of angiotensin II (N=30) and methoxamine (N=10) in normal individuals. Serial measurements of left ventricular dimensions and wall thickness were performed by M-mode echocardiography; the end-systolic pressure was assessed by indirect, calibrated carotid pulse tracings. The end-diastolic dimension, which reflects preload, remained unchanged during the afterload challenge using angiotensin II, but increased significantly using methoxamine (P < 0.001). Significant differences due to the agent used were observed for the end-systolic pressure-dimension relationship (P < 0.0002), the relation between end-systolic wall stress and fractional shortening (P < 0.002), and the relation between end-systolic wall stress and mean fibre shortening velocity (P < 0.02). The extrapolated end-systolic dimension Do at zero end-systolic pressure was significantly shifted to the left when using angiotensin II (P < 0.02); this is considered to be due to its negligible effect on preload. Our data suggest that the assessment of the end-systolic pressure-dimension and stress-shortening relationships depends significantly on drug specific effects and the variation of preload during the afterload challenge. Based on these results, the use of angiotensin II is emphasized for the assessment of the end-systolic pressure-dimension and stress-shortening relationships.