Consolini A E, Marquez M T, Ponce-Hornos J E
Instituto de Investigaciones Cardiológicas, Facultad de Medicina y Cátedra de Biofísica, Facultad de Odontología, Universidad de Buenos Aires-CONICET, Argentina.
Can J Physiol Pharmacol. 2001 Jul;79(7):551-8.
Heat production under no-flow ischemia (ISCH) and under hypoperfusion (HYP) conditions was measured in single isovolumetric contractions of perfused rat ventricles at 25 degrees C. Resting heat production (Hr) and resting pressure decreased when the perfusion rate was reduced from 6 to 1.5 mL min(-1) or lower flows (HYP) and by ISCH. Maximal developed pressure (P) decreased to 29% and 20% of control by HYP at 0.8 mL min(-1) and ISCH, respectively. The tension-independent heat (TIH) fraction attributed to Ca2+-binding, measured during single contractions, decreased under HYP with an increase in the ratio between the maximum relaxation rate and P (-P/P ratio). The TIH fractions (attributed to Ca2+ binding and Ca2+ removal processes) decreased under ISCH. The long duration TIH fraction associated with Ca2+-dependent mitochondrial activity disappeared at flow rates of 1.5 mL min(-1) or lower. The ratio between the tension-dependent energy release and P was decreased by ISCH but not by HYP, indicating that under ISCH there was an improvement in contractile economy, but this was not modified by HYP. Overall, the results indicate that no-flow and low-flow ischemias are energetically different models. While the contractile failure under HYP seems to be related to a decrease in myofilament Ca2+ sensitivity, under ISCH it appears to be related to decreased cytosolic Ca2+ availability combined with a more noticeable effect on a fraction of energy that has been attributed to mitochondrial activity. Furthermore, mechanical and energetic responses of both models (i.e., ISCH and HYP) found in the present work were not the same as those previously observed in severe hypoxia so that all these models should not be used indistinctly.
在25摄氏度下，对灌注大鼠心室的单次等容收缩过程中无血流缺血（ISCH）和低灌注（HYP）条件下的产热进行了测量。当灌注速率从6降至1.5 mL min⁻¹或更低流量（HYP）以及发生ISCH时，静息产热（Hr）和静息压力降低。在0.8 mL min⁻¹的HYP和ISCH条件下，最大发展压力（P）分别降至对照值的29%和20%。在单次收缩过程中测量的归因于Ca²⁺结合的张力非依赖性热（TIH）部分，在HYP条件下随着最大舒张速率与P的比值（-P/P比值）增加而降低。TIH部分（归因于Ca²⁺结合和Ca²⁺清除过程）在ISCH条件下降低。与Ca²⁺依赖性线粒体活性相关的长时间TIH部分在1.5 mL min⁻¹或更低的流速下消失。ISCH降低了张力依赖性能量释放与P的比值，但HYP未使其降低，这表明在ISCH条件下收缩经济性有所改善，但HYP未对其产生影响。总体而言，结果表明无血流和低血流缺血是能量学上不同的模型。虽然HYP条件下的收缩功能衰竭似乎与肌丝Ca²⁺敏感性降低有关，但在ISCH条件下，它似乎与胞质Ca²⁺可用性降低以及对一部分归因于线粒体活性的能量产生更显著的影响有关。此外，本研究中发现的这两种模型（即ISCH和HYP）的机械和能量学反应与先前在严重缺氧中观察到的不同，因此不应不加区分地使用所有这些模型。
