Shimizu M, Kimura S, Myerburg R J, Bassett A L
Department of Pharmacology, University of Miami School of Medicine, FL 33101.
J Mol Cell Cardiol. 1990 Jun;22(6):697-705. doi: 10.1016/0022-2828(90)91012-v.
This study was designed to examine the effects of hypoxia, acidosis, glucose-free medium and their combination on contraction and sarcoplasmic reticulum (SR) function in rat ventricular trabeculae. The isometric twitch tension was measured during superfusion with hypoxic (PO2 less than 30 mmHg), acidic (pH 6.80), glucose-free, or their combined ("ischemic") Tyrode's solution at 20 degrees C. The time needed to fully recover the contraction induced by 10 mM caffeine (repriming time) was measured to indirectly estimate the Ca2+ uptake of the SR. In "ischemia" and acidosis, the peak developed tension decreased progressively for the first 30 min (37.6 +/- 9.2% and 56.6 +/- 8.4% of control at 30 min, respectively), and then became steady. In hypoxic solution, the peak developed tension decreased moderately for the first 30 min (86.8 +/- 4.8% of control at 30 min), and thereafter remained steady. Developed tension did not change significantly during 60 min of superfusion with glucose-free solution. The repriming time of caffeine contraction was significantly delayed in both "ischemic" and hypoxic solutions, but was unchanged in acidic and glucose-free solutions. These results lead us to suggest that depressed SR function to accumulate Ca2+ may contribute to the decline in tension in ischemia and hypoxia, but that other mechanisms are important in the tension decline induced by acidosis.
本研究旨在探讨缺氧、酸中毒、无糖培养基及其组合对大鼠心室肌小梁收缩和肌浆网（SR）功能的影响。在20℃下，用缺氧（PO2小于30 mmHg）、酸性（pH 6.80）、无糖或其组合（“缺血”）的台氏液进行灌流时，测量等长收缩张力。测量10 mM咖啡因诱导的收缩完全恢复所需的时间（复灌时间），以间接估计SR的Ca2+摄取。在“缺血”和酸中毒时，前30分钟内最大张力峰值逐渐降低（30分钟时分别为对照的37.6±9.2%和56.6±8.4%），然后趋于稳定。在缺氧溶液中，前30分钟内最大张力峰值适度降低（30分钟时为对照的86.8±4.8%），此后保持稳定。用无糖溶液灌流60分钟期间，最大张力无明显变化。咖啡因收缩的复灌时间在“缺血”和缺氧溶液中均显著延迟，但在酸性和无糖溶液中无变化。这些结果表明，SR功能降低导致Ca2+蓄积可能是缺血和缺氧时张力下降的原因，但其他机制在酸中毒诱导的张力下降中也很重要。
