Hoffmeister H M, Storf R, Thiedemann K U, Seipel L
Medizinische Klinik, University of Tübingen, FRG.
Basic Res Cardiol. 1989 Jan-Feb;84(1):77-90. doi: 10.1007/BF01907005.
To investigate myocardial performance and diastolic properties after repeated periods of oxygen deficiency auxotonic and isovolumic measurements were performed after three periods (4 min) of asphyxia in Wistar rats (n = 19). Additionally, the response of the peak isovolumic left ventricular pressure to postextrasystolic potentiation was measured. The hemodynamic results were compared to the levels of high-energy phosphates. Already after 15 min of recovery from asphyxia auxotonic measures of systolic function were completely normal compared to the control group (n = 19). Isovolumic measurements after 20 min of postasphyctic recovery, however, demonstrated a considerable reduction of the peak left ventricular pressure (226.5 +/- 7.5 mm Hg vs. 262.6 +/- 3.4 mm Hg in controls, mean +/- SEM (p less than 0.01) indicating persistence of decreased postischemic contractile performance. The relative effect of postextrasystolic potentiation was similar in both groups, but could not compensate for the reduced performance of the postasphyctic hearts: the absolute postextrasystolic peak isovolumic pressure of the postasphyctic hearts was lower than the value of the regular isovolumic peak pressure in the controls. Diastolic properties (pressure/volume and stress/strain relationships) of the postasphyctic myocardium remained unchanged. The total sum of the adenine-nucleotides decreased from 7.2 +/- 0.2 to 5.6 +/- 0.3 mumol/gww (p less than 0.01). ATP was reduced from 4.8 +/- 0.2 to 3.9 +/- 0.3 mumol/gww (p less than 0.01). Phosphocreatine was elevated to 7.0 +/- 0.6 mumol/gww, x +/- SEM (p less than 0.01). Our results demonstrated normal postasphyctic basal hemodynamics and material properties. Thus, the energy supply was sufficient to maintain steady state conditions - in spite of decreased overall adenine-nucleotide levels. Isovolumic measurements and postextrasystolic potentation tests, however, indicated that the contractile performance of the postischemic myocardium was still reduced. This functional limitation cannot be explained by altered material properties and is probably not causally related to the decreased overall ATP content.
为研究反复缺氧后的心肌性能和舒张特性，对19只Wistar大鼠进行了三期（4分钟）窒息后进行了辅助张力和等容测量。此外，还测量了等容左心室压力峰值对早搏后增强的反应。将血流动力学结果与高能磷酸盐水平进行比较。与对照组（n = 19）相比，窒息复苏15分钟后，收缩功能的辅助张力测量已完全正常。然而，窒息后恢复20分钟后的等容测量显示左心室压力峰值显著降低（对照组为262.6 +/- 3.4 mmHg，窒息组为226.5 +/- 7.5 mmHg，平均值 +/- 标准误，p < 0.01），表明缺血后收缩性能持续下降。早搏后增强的相对效应在两组中相似，但无法弥补窒息后心脏性能的降低：窒息后心脏的早搏后等容峰值压力绝对值低于对照组正常等容峰值压力值。窒息后心肌的舒张特性（压力/容积和应力/应变关系）保持不变。腺嘌呤核苷酸的总量从7.2 +/- 0.2降至5.6 +/- 0.3 μmol/gww（p < 0.01）。ATP从4.8 +/- 0.2降至3.9 +/- 0.3 μmol/gww（p < 0.01）。磷酸肌酸升高至7.0 +/- 0.6 μmol/gww，x +/- 标准误（p < 0.01）。我们的结果表明窒息后基础血流动力学和物质特性正常。因此，尽管腺嘌呤核苷酸总体水平降低，但能量供应足以维持稳态条件。然而，等容测量和早搏后增强试验表明，缺血后心肌的收缩性能仍然降低。这种功能限制无法用物质特性改变来解释，可能与总ATP含量降低没有因果关系。
